MicroRNA-34a functions as a potential tumor suppressor by inducing apoptosis in neuroblastoma cells
|
|
- Preston Horn
- 6 years ago
- Views:
Transcription
1 SHORT COMMUNICATION MicroRNA-34a functions as a potential tumor suppressor by inducing apoptosis in neuroblastoma cells C Welch, Y Chen and RL Stallings (2007) 26, & 2007 Nature Publishing Group All rights reserved /07 $ Children s Cancer Research Institute and Department of Pediatrics, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA Neuroblastoma (NB) is one of the most common forms of cancer in children, accountingfor 15% of pediatric cancer deaths. The clinical course of these tumors is highly variable and is dependent on such factors as age at presentation, stage, ploidy and genomic abnormalities. Hemizygous deletion of chromosome 1p occurs in approximately 30% of advanced stage tumors, is associated with a poor prognosis, and likely leads to the loss of one or more tumor suppressor genes. We show here that microrna (mirna)-34a (1p36.23) is generally expressed at lower levels in unfavorable primary NB tumors and cell lines relative to normal adrenal tissue and that reintroduction of this mirna into three different NB cell lines causes a dramatic reduction in cell proliferation through the induction of a caspase-dependent apoptotic pathway. As a potential mechanistic explanation for this observation, we demonstrate that mir-34a directly targets the messenger ribonucleic acid (mrna) encoding E2F3 and significantly reduces the levels of E2F3 protein, a potent transcriptional inducer of cell-cycle progression. Furthermore, mir-34a expression increases duringretinoic acidinduced differentiation of the SK-N-BE cell line, whereas E2F3 protein levels decrease. Thus, addingto the increasingrole of mirnas in cancer, mir-34a may act as a suppressor of NB tumorgenesis. (2007) 26, ; doi: /sj.onc ; published online 12 February 2007 Keywords: apoptosis; CGH; E2F3; microrna; neuroblastoma; tumour suppressors Neuroblastoma (NB) is a pediatric tumor originating from precursor cells of the sympathetic nervous system. These tumors account for 15% of childhood cancer deaths and are particularly noted for a wide range in clinical behavior, ranging from spontaneous regression to rapid progression and death owing to disease (Brodeur, 2003). Loss of chromosome 1p material, Correspondence: Professor RL Stallings, Children s Cancer Research Institute and Department of Pediatrics, University of Texas Health Science Center at San Antonio, 8403 Floyd Curl Drive, MC 7784, San Antonio, TX, USA. STALLINGS@uthscsa.edu Received 6 October 2006; revised 1 December 2006; accepted 13 December 2006; published online 12 February 2007 occurring predominately through an unbalanced t(1;17) that also results in gain of 17q (Van Roy et al., 1994), is a common chromosomal imbalance found in NB and occurs preferentially in tumors with MYCN amplification (MNA) (Fong et al., 1989). All three of these nonrandom genetic abnormalities, loss of 1p, gain of 17q and MNA, are independently associated with a poor clinical outcome (Brodeur et al., 1984; Spitz et al., 2003; Attiyeh et al., 2005; Vandesompele et al., 2005). Although the importance of 1p loss in NB pathogenesis has been known for some time, the genes and genetic pathways affected by this loss are not completely understood. The region of 1p loss is quite large, containing many potential candidate genes. Furthermore, smaller homozygous deletions that might further pinpoint the genes of interest are exceedingly rare (Mosse et al., 2005; Stallings et al., 2006) and do not define a single shortest region of overlap (Schleiermacher et al., 1994). Expression microarray studies of primary tumors have also led some investigators to suggest that multiple genes on chromosome 1p contribute to NB pathogenesis (Janoueix-Lerosey et al., 2004; Wang et al., 2006), a concept supported by the fact that in vitro functional studies have shown that more than one gene from chromosome 1p can have anti-tumorigenic effects when ectopically expressed in NB cell lines (Ejeskar et al., 2005; Valentijn et al., 2005). Here, we explore the possibility that some of the chromosome 1p sequences with tumor suppressor effects in NB are not conventional protein coding gene sequences, but rather micrornas (mirnas), which regulate gene expression at a post-transcriptional level by either inhibiting mrnas from being translated or causing them to be degraded. MiRNAs play major roles in the differentiation of neural cells (Miska, 2005), and the dysregulation of these sequences can have tumor suppressor or oncogenic activity in different forms of cancer (Esquela-Kerscher and Slack, 2006). For example, two mirnas (mir-15 and mir-16) mapping to chromosomal region 13q14 are frequently deleted and downregulated in chronic lymphocytic leukemia and thus act as tumor suppressor genes (Calin et al., 2002). MiRNAs acting in a dominant oncogenic manner are illustrated by mir-21 on chromosome 17q, which, when overexpressed in some forms of cancer have anti
2 5018 Figure 1 Analysis of 1p loss in 13 primary tumors and the SK-N-AS cell line using oligonucleotide array CGH, as described previously (Stallings et al., 2006). The vertical axis of each plot represents the fluorescence ratio of tumor to normal DNA on a log 2 scale, whereas the horizontal axis represents genomic position on chromosome 1p in base pairs. The array CGH data was generated by NimbleGen Systems Inc (Iceland). Positions of mir-34a and mir-30e are noted at the top of the figure. Chromosome 1p breakpoints are denoted with arrows.
3 5019 Figure 2 Reverse transcriptase QPCR expression analysis of mir-34a in low stage hyperdiploid tumors with favorable histopathology (grey), high stage 11q- tumors with unfavorable histopathology (clear), high stage MYCN amplified tumors with unfavorable histopathology (black), NB cell lines Kelly, SK-N-AS, NGP, SK-N-BE and adrenal gland (dark grey). Reverse transcription with stemloop primers was carried out as described by Chen et al. (2005) (Supplementary methods). Samples designated with an * have 1p loss. apoptotic effects (Chan et al., 2005; Cimmino et al., 2005). An in silico search for mirnas encoded within the 1p region identified mir-34a (1p36.23) and mir-30e (1p34.2) as potential candidates. Using array comparative genomic hybridization (CGH) data on a published set of tumors, we determined that the region encoding mir-34a is located in the minimal region of 1p loss (Figure 1) whereas the region encoding mir-30e is lost in 79% of tumors (Stallings et al., 2006). Using realtime PCR analysis, the expression of mir-34a was generally reduced in NB primary tumors as compared to normal adrenal gland (Figure 2), and tumors with 1p loss have a 30% reduction in mir-34a expression relative to tumors with an intact 1p locus. Similarly, mir-34a expression is reduced in the majority of NB cell lines tested. Initially, we determined if ectopic expression of either mir-30e or mir-34a had a biological effect in three different NB cell lines, two with MNA (Kelly, NGP) and one lacking MNA (SK-N-AS), using the 3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) cell viability assay. Each cell line transfected with pre-mir-34a had a significant reduction in metabolically active cells compared with the scrambled negative control over a 5-day interval (Figure 3a). A reduction in cell viability was detected in each cell line by day 2 following transfection, and dramatic loss of cell viability was apparent by day 5. In contrast, transfection of cell lines with mir-30e had no effect on cell viability even though its expression was at the same level as mir-34a, as evaluated by real-time quantitative polymerase chain reaction (data not shown). To determine the possible mechanism of the antiproliferative activity of mir-34a, activation of the caspase 3/7 apoptotic pathway was assessed following transfection of pre-mir-34a into each cell line. Caspase- 3 and -7 enzymatic activities (key executioners of apoptosis) significantly increased by 72 h post-transfection in Kelly cells treated with pre-mir-34a relative to the scrambled RNA transfected control cells Figure 3 (a) MTT cell viability assay, as described in the Supplementary methods, was performed on days 1 to 5 after Lipofectamine transfection of Kelly, NGP and SK-N-AS cells with either a pre-mir-34a molecule (10 nm) or a negative control scrambled oligonucleotide that does not encode for any known mirna (Ambion). Cell populations transfected with the negative control oligo had a significantly greater number of metabolically active cells than cells transfected with the pre-mir-34a. (b) Caspase 3/7 assay, as described in the Supplementary methods, was carried out on Kelly, NGP and SK-N-AS cells transfected with either the negative control oligo (dark grey) or the pre-mir-34a (diagonal stripe). Kelly showed a maximal effect at day 3, whereas the other two cell lines showed the greatest effect on day 5. Statistical significance for caspase-3/7 activity was assessed using a Student s paired t-test.
4 5020 Figure 4 (a) Validation of mir-34a mrna targets. Luciferase constructs were made by ligating oligonucleotides containing the putative target site into the XbaI site of the pgl3-control vector (promega) as described previously (Guo et al., 2006) (see Supplementary methods). A significant reduction in luciferase activity is detected when an oligonucleotide containing the exact complementary sequence of mir-34a is cloned into the construct (pgl3_mir-34a). Neither the construct containing the putative MYCN target sequence (pgl3_mycn oligo) or a 625 bp fragment of the 3-UTR (pgl3_mycn UTR) showed a reduction in luciferase activity, indicating that MYCN is not a direct target of mir-34a. There was a significant reduction in luciferase activity when synthesized oligonucleotides representing the putative E2F3 3-UTR target site was used (pgl3_e2f3 oligo). This effect was abolished when a sequence containing a mutated seed site was used (pgl3_e2f3 mut). (b) Effect of mir-34a expression on endogenous E2F3 levels. The SK-N-AS cell line was transfected with 10 nm mir-34a precursor molecule or a negative control precursor mirna. E2F3 protein levels were determined by Western blot of nuclear extracts isolated on day 3 post-transfection (Supplementary methods). Relative to the negative control mirna, mir-34a expression significantly reduced the levels of E2F3. (c) Effect of ATRA on mir-34a expression following treatment and differentiation of NB SK-N-BE cell line. The graph shows relative mir-34a expression using quantitative realtime PCR, as described in Figure 2. The cells treated with 5 or 10 mm ATRA displayed morphological changes such as neuritic extensions that were indicative of a differentiated state. MiR-34a expression increased 2 to 2.5-fold in SK-N-BE cells. It is important to note that SK-N-BE cells have hemizygous loss of the 1p region, so that presumably the fold induction of mir-34a would be twofold higher in cells having two copies of this locus. (d) Effect of ATRA treatment on endogenous E2F3 levels. Western blot analysis of E2F3 was performed on SK-N-BE nuclear extracts following 6 days of ATRA treatment. Differentiated SK-N-BE cells show a marked reduction in E2F3 levels. (Figure 3b). The maximum increase in caspase 3/7 activity in NGP and SK-N-AS cells occurred at day 5 post-transfection. Endogenous mir-34a expression, which is B50 fold higher in Kelly than in the other two cell lines (Figure 2), might explain why mir-34a has an earlier effect in this cell line. Computational predictions for human mrna targets of mir-34a indicated numerous potential candidates, as detailed at miranda ( sequences), TargetScan ( and PicTar ( Two of the more significant putative targets in the context of NB were MYCN and E2F3, which are conserved between humans and rodents. To validate whether mir-34a directly recognizes the 3 0 -UTR of these transcripts, we cloned oligonucleotides representing the presumed target sites (Supplementary Table 1) into the 3 0 -UTR of the luciferase gene and luciferase levels were compared in SK-N-AS cells cotransfected with one of these constructs and a pre-mir-34a or a negative control RNA. As a positive control, a luciferase construct was created that contains the complete complementary sequence to mir-34a. The overexpression of mir-34a had no effect on either the oligonucleotide construct representing the MYCN 3 0 UTR or on a construct containing 625 bp of the MYCN 3 0 UTR, indicating that MYCN is not a mir-34a target. In contrast, overexpression of mir-34a reduced the luciferase activity from the reporter construct containing the E2F3 site and the positive control (Figure 4a), whereas no effect was observed with a construct containing a mutated E2F3 seed site (Figure 4a). This effect was specific because there was no change in luciferase reporter activity when a negative control scrambled mirna was cotransfected with either reporter construct (Figure 4a). These results suggest that the complementary site in the E2F3 mrna is a target of mir-34amediated post-transcriptional gene silencing. Western blot analysis of SK-N-AS cells transfected with mir-34a showed a significant reduction in E2F3 protein in cells
5 overexpressing mir-34a, confirming that mir-34a targets E2F3 mrna (Figure 4b) All trans-retinoic acid (ATRA) induces the terminal differentiation of NB cells (Thiele et al., 1985). To test whether mir-34a is induced during the differentiation process, we analysed the expression level of mir-34a in SK-N-BE cells treated with ATRA. ATRA induced the dose-dependent expression of mir-34a following differentiation (Figure 4c). As predicted, Western blot analysis showed a significant reduction of E2F3 protein in SK-N-BE cells treated with ATRA relative to untreated cells (Figure 4d). This result suggests that the drop in E2F3 levels following ATRA treatment may be owing to the increase in expression of mir-34a. In summary, we demonstrate that mir-34a has tumor suppressor activity when ectopically expressed in NB cell lines through induction of a caspase 3/7 apoptotic References Attiyeh EF, London WB, Mosse YP, Wang Q, Winter C, Khazi D et al. (2005). Chromosome 1p and 11q deletions and outcome in neuroblastoma. N Engl J Med 353: Brodeur GM. (2003). Neuroblastoma: biological insights into a clinical enigma. Nat Rev Cancer 3: Brodeur GM, Seeger RC, Schwab M, Varmus HE, Bishop JM. (1984). Amplification of N-myc in untreated human neuroblastomas correlates with advanced disease stage. Science 224: Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, Noch E et al. (2002). Frequent deletions and down-regulation of micro- RNA genes mir15 and mir16 at 13q14 in chronic lymphocytic leukemia. Proc Natl Acad Sci USA 99: Calin GA, Ferracin M, Cimmino A, Di Leva G, Shimizu M, Wojcik SE et al. (2005). A MicroRNA signature associated with prognosis and progression in chronic lymphocytic leukemia. N Engl J Med 353: Chan JA, Krichevsky AM, Kosik KS. (2005). MicroRNA-21 is an antiapoptotic factor in human glioblastoma cells. Cancer Res 65: Chen C, Ridzon DA, Broomer AJ, Zhou Z, Lee DH, Nguyen JT et al. (2005). Real-time quantification of micrornas by stem-loop RT-PCR. Nucleic Acids Res 33: e179. Cimmino A, Calin GA, Fabbri M, Iorio MV, Ferracin M, Shimizu M et al. (2005). mir-15 and mir-16 induce apoptosis by targeting BCL2. Proc Natl Acad Sci USA 102: Ejeskar K, Krona C, Caren H, Zaibak F, Li L, Martinsson T et al. (2005). Introduction of in vitro transcribed ENO1 mrna into neuroblastoma cells induces cell death. BMC Cancer 5: 161. Esquela-Kerscher A, Slack FJ. (2006). Oncomirs - micrornas with a role in cancer. Nat Rev Cancer 6: Fong CT, Dracopoli NC, White PS, Merrill PT, Griffith RC, Housman DE et al. (1989). Loss of heterozygosity for the short arm of chromosome 1 in human neuroblastomas: correlation with N-myc amplification. Proc Natl Acad Sci USA 86: Guo Y, Chen Y, Ito H, Watanabe A, Ge X, Kodama T et al. (2006). Identification and characterization of lin-28homolog B (LIN28B) in human hepatocellular carcinoma. Gene 384: pathway. MiR-34a may have an antiproliferative effect, in part, through targeting the E2F3 transcription factor. Recently, it has been shown that mir-17-5p and mir-20a, which are part of the mir-17 cluster on chromosome 13, act as tumor suppressors by targeting and reducing E2F1 levels (O Donnell et al., 2005). Similar to mir-34a, the region harboring the mir-17 cluster is hemizygously deleted in some human tumors (Lin et al., 1999). This same region, however, is amplified in diffuse large B-cell lymphoma samples (Calin et al., 2005; He et al., 2005). Thus, as suggested previously (O Donnell et al., 2005), mirnas may exert a tumor suppressor or oncogenic effect depending upon the cell type in which they are expressed. In this regard, it is interesting to note that E2F family members can have both cell proliferative and proapoptotic effects in different cellular contexts (Johnson and Degregori, 2006). He L, Thomson JM, Hemann MT, Hernando-Monge E, Mu D, Goodson S et al. (2005). A microrna polycistron as a potential human oncogene. Nature 435: Janoueix-Lerosey I, Novikov E, Monteiro M, Gruel N, Schleiermacher G, Loriod B et al. (2004). Gene expression profiling of 1p35-36 genes in neuroblastoma. 23: Johnson DG, Degregori J. (2006). Putting the Oncogenic and Tumor Suppressive Activities of E2F into Context. Curr Mol Med 6: Lin YW, Sheu JC, Liu LY, Chen CH, Lee HS, Huang GT et al. (1999). Loss of heterozygosity at chromosome 13q in hepatocellular carcinoma: identification of three independent regions. Eur J Cancer 35: Miska EA. (2005). How micrornas control cell division, differentiation and death. Curr Opin Genet Dev 15: Mosse YP, Greshock J, Margolin A, Naylor T, Cole K, Khazi D et al. (2005). High-resolution detection and mapping of genomic DNA alterations in neuroblastoma. Genes Chromosomes Cancer 43: O Donnell KA, Wentzel EA, Zeller KI, Dang CV, Mendell JT. (2005). c-myc-regulated micrornas modulate E2F1 expression. Nature 435: Schleiermacher G, Peter M, Michon J, Hugot JP, Vielh P, Zucker JM et al. (1994). Two distinct deleted regions on the short arm of chromosome 1 in neuroblastoma. Genes Chromosomes Cancer 10: Spitz R, Hero B, Ernestus K, Berthold F. (2003). Deletions in chromosome arms 3p and 11q are new prognostic markers in localized and 4 s neuroblastoma. Clin Cancer Res 9: Stallings RL, Nair P, Maris JM, Catchpoole D, McDermott M, O Meara A et al. (2006). High-resolution analysis of chromosomal breakpoints and genomic instability identifies PTPRD as a candidate tumor suppressor gene in neuroblastoma. Cancer Res 66: Thiele CJ, Reynolds CP, Israel MA. (1985). Decreased expression of N-myc precedes retinoic acid-induced morphological differentiation of human neuroblastoma. Nature 313: Valentijn LJ, Koppen A, van Asperen R, Root HA, Haneveld F, Versteeg R. (2005). Inhibition of a new differentiation pathway in neuroblastoma by copy number 5021
6 5022 defects of N-myc, Cdc42, and nm23 genes. Cancer Res 65: Van Roy N, Laureys G, Cheng NC, Willem P, Opdenakker G, Versteeg R et al. (1994). 1;17 translocations and other chromosome 17 rearrangements in human primary neuroblastoma tumors and cell lines. Genes Chromosomes Cancer 10: Vandesompele J, Baudis M, De Preter K, Van Roy N, Ambros P, Bown N et al. (2005). Unequivocal delineation of clinicogenetic subgroups and development of a new model for improved outcome prediction in neuroblastoma. J Clin Oncol 23: Wang Q, Diskin S, Rappaport E, Attiyeh E, Mosse Y, Shue D et al. (2006). Integrative genomics identifies distinct molecular classes of neuroblastoma and shows that multiple genes are targeted by regional alterations in DNA copy number. Cancer Res 66: Supplementary Information accompanies the paper on the website (
mirna Dr. S Hosseini-Asl
mirna Dr. S Hosseini-Asl 1 2 MicroRNAs (mirnas) are small noncoding RNAs which enhance the cleavage or translational repression of specific mrna with recognition site(s) in the 3 - untranslated region
More informationSoft Agar Assay. For each cell pool, 100,000 cells were resuspended in 0.35% (w/v)
SUPPLEMENTARY MATERIAL AND METHODS Soft Agar Assay. For each cell pool, 100,000 cells were resuspended in 0.35% (w/v) top agar (LONZA, SeaKem LE Agarose cat.5004) and plated onto 0.5% (w/v) basal agar.
More informationProfiles of gene expression & diagnosis/prognosis of cancer. MCs in Advanced Genetics Ainoa Planas Riverola
Profiles of gene expression & diagnosis/prognosis of cancer MCs in Advanced Genetics Ainoa Planas Riverola Gene expression profiles Gene expression profiling Used in molecular biology, it measures the
More informationMicroRNA expression profiling and functional analysis in prostate cancer. Marco Folini s.c. Ricerca Traslazionale DOSL
MicroRNA expression profiling and functional analysis in prostate cancer Marco Folini s.c. Ricerca Traslazionale DOSL What are micrornas? For almost three decades, the alteration of protein-coding genes
More informationCircular RNAs (circrnas) act a stable mirna sponges
Circular RNAs (circrnas) act a stable mirna sponges cernas compete for mirnas Ancestal mrna (+3 UTR) Pseudogene RNA (+3 UTR homolgy region) The model holds true for all RNAs that share a mirna binding
More informationmicrornas (mirna) and Biomarkers
micrornas (mirna) and Biomarkers Small RNAs Make Big Splash mirnas & Genome Function Biomarkers in Cancer Future Prospects Javed Khan M.D. National Cancer Institute EORTC-NCI-ASCO November 2007 The Human
More informationChapter 4 Cellular Oncogenes ~ 4.6 -
Chapter 4 Cellular Oncogenes - 4.2 ~ 4.6 - Many retroviruses carrying oncogenes have been found in chickens and mice However, attempts undertaken during the 1970s to isolate viruses from most types of
More informationa) List of KMTs targeted in the shrna screen. The official symbol, KMT designation,
Supplementary Information Supplementary Figures Supplementary Figure 1. a) List of KMTs targeted in the shrna screen. The official symbol, KMT designation, gene ID and specifities are provided. Those highlighted
More informationResearch Communication
IUBMB Life, 64(7): 628 635, July 2012 Research Communication MicroRNA-181b Targets camp Responsive Element Binding Protein 1 in Gastric Adenocarcinomas Lin Chen*, Qian Yang*, Wei-Qing Kong*, Tao Liu, Min
More informationInhibition of the Growth of Raji Cells by Precursor MicroRNA-15a
22 Clin Oncol Cancer Res (2010) 7: 22-26 DOI 10.1007/s11805-010-0022-1 Inhibition of the Growth of Raji Cells by Precursor MicroRNA-15a Dong-mei HE Qin CHEN Institute of Hematology, Medical College of
More informationBerberine Sensitizes Human Ovarian Cancer Cells to Cisplatin Through mir-93/ PTEN/Akt Signaling Pathway
Chen Accepted: et al.: February Berberine 24, Sensitizes 2015 Ovarian Cancer Cells to Cisplatin www.karger.com/cpb 956 1421-9778/15/0363-0956$39.50/0 Original Paper This is an Open Access article licensed
More informationAssociation of microrna 21 With Biological Features and Prognosis of Neuroblastoma
Special Report Association of microrna 21 With Biological Features and Prognosis of Neuroblastoma Yaodong Zhou, MD, and Bo Sheng, MD Background: The aim of this study was to assess the differences in microrna
More informationMicroRNA Cancer qpcr Array
MicroRNA Cancer qpcr Array Array Layout Pre-designed set of 95 MicroRNA detection Primers U6 snrna Normalization transcript Selection of Candidate MicroRNAs for Cancer Array Sample References of MicroRNA
More informationmicrorna-200b and microrna-200c promote colorectal cancer cell proliferation via
Supplementary Materials microrna-200b and microrna-200c promote colorectal cancer cell proliferation via targeting the reversion-inducing cysteine-rich protein with Kazal motifs Supplementary Table 1.
More informationBIO360 Fall 2013 Quiz 1
BIO360 Fall 2013 Quiz 1 1. Examine the diagram below. There are two homologous copies of chromosome one and the allele of YFG carried on the light gray chromosome has undergone a loss-of-function mutation.
More informationChromosome 1p and 11q Deletions and Outcome in Neuroblastoma
original article Chromosome 1p and 11q Deletions and Outcome in Neuroblastoma Edward F. Attiyeh, M.D., Wendy B. London, Ph.D., Yael P. Mossé, M.D., Qun Wang, M.D., Ph.D., Cynthia Winter, B.A., Deepa Khazi,
More informationMicro RNA Research. Ken Kosik. Harriman Professor, Department of Molecular, Cellular & Developmental Biology and Biomolecular Sciences & Engr.
Ken Kosik Harriman Professor, Department of Molecular, Cellular & Developmental Biology and Biomolecular Sciences & Engr. Program Co-Director, Neurosciences Research Institute Micro RNA Research Neuroscience
More informationMicroRNA and Male Infertility: A Potential for Diagnosis
Review Article MicroRNA and Male Infertility: A Potential for Diagnosis * Abstract MicroRNAs (mirnas) are small non-coding single stranded RNA molecules that are physiologically produced in eukaryotic
More informationLentiviral Delivery of Combinatorial mirna Expression Constructs Provides Efficient Target Gene Repression.
Supplementary Figure 1 Lentiviral Delivery of Combinatorial mirna Expression Constructs Provides Efficient Target Gene Repression. a, Design for lentiviral combinatorial mirna expression and sensor constructs.
More informationT H E J O U R N A L O F C E L L B I O L O G Y
T H E J O U R N A L O F C E L L B I O L O G Y Supplemental material Amelio et al., http://www.jcb.org/cgi/content/full/jcb.201203134/dc1 Figure S1. mir-24 regulates proliferation and by itself induces
More informationHepatitis B virus X gene in the development of hepatocellular carcinoma. Citation Hong Kong Medical Journal, 2011, v. 17 n. 6, suppl. 6, p.
Title Hepatitis B virus X gene in the development of hepatocellular carcinoma Author(s) Ma, NF; Lau, SH; Hu, L; Dong, SS; Guan, XY Citation Hong Kong Medical Journal, 2011, v. 17 n. 6, suppl. 6, p. 44-47
More informationMicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells
MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells Margaret S Ebert, Joel R Neilson & Phillip A Sharp Supplementary figures and text: Supplementary Figure 1. Effect of sponges on
More informationHigh AU content: a signature of upregulated mirna in cardiac diseases
https://helda.helsinki.fi High AU content: a signature of upregulated mirna in cardiac diseases Gupta, Richa 2010-09-20 Gupta, R, Soni, N, Patnaik, P, Sood, I, Singh, R, Rawal, K & Rani, V 2010, ' High
More informationSUPPLEMENTARY FIGURES AND TABLES
SUPPLEMENTARY FIGURES AND TABLES Supplementary Figure S1: CaSR expression in neuroblastoma models. A. Proteins were isolated from three neuroblastoma cell lines and from the liver metastasis of a MYCN-non
More informationmicrorna Presented for: Presented by: Date:
microrna Presented for: Presented by: Date: 2 micrornas Non protein coding, endogenous RNAs of 21-22nt length Evolutionarily conserved Regulate gene expression by binding complementary regions at 3 regions
More informationMicroRNA dysregulation in cancer. Systems Plant Microbiology Hyun-Hee Lee
MicroRNA dysregulation in cancer Systems Plant Microbiology Hyun-Hee Lee Contents 1 What is MicroRNA? 2 mirna dysregulation in cancer 3 Summary What is MicroRNA? What is MicroRNA? MicroRNAs (mirnas) -
More informationMicroRNAs: the primary cause or a determinant of progression in leukemia?
MicroRNAs: the primary cause or a determinant of progression in leukemia? The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation
More informationThe Role of ploidy in neuroblastoma. Michael D. Hogarty, MD Division of Oncology Children s Hospital of Philadelphia
The Role of ploidy in neuroblastoma Reprinted from NB Journal Summer Issue 2003 Children s Neuroblastoma Cancer Foundation Michael D. Hogarty, MD Division of Oncology Children s Hospital of Philadelphia
More informationSupplementary Appendix
Supplementary Appendix This appendix has been provided by the authors to give readers additional information about their work. Supplement to: Bredel M, Scholtens DM, Yadav AK, et al. NFKBIA deletion in
More information10/31/2017. micrornas and cancer. From the one gene-one enzyme hypothesis to. microrna DNA RNA. Transcription factors.
micrornas and cancer Cellular and Molecular Biology of Cancer (PATH G4500-001) November 1 st, 2017 -Katia Basso- Columbia University Katia Basso, PhD Office: ICRC RM506 E-mail: kb451@cumc.columbia.edu
More informationA novel and universal method for microrna RT-qPCR data normalization
A novel and universal method for microrna RT-qPCR data normalization Jo Vandesompele professor, Ghent University co-founder and CEO, Biogazelle 4 th International qpcr Symposium Weihenstephan, March 1,
More informationSupplementary Figure 1
Supplementary Figure 1 Asymmetrical function of 5p and 3p arms of mir-181 and mir-30 families and mir-142 and mir-154. (a) Control experiments using mirna sensor vector and empty pri-mirna overexpression
More informationPredicting clinical outcomes in neuroblastoma with genomic data integration
Predicting clinical outcomes in neuroblastoma with genomic data integration Ilyes Baali, 1 Alp Emre Acar 1, Tunde Aderinwale 2, Saber HafezQorani 3, Hilal Kazan 4 1 Department of Electric-Electronics Engineering,
More informationMolecular Diagnosis. Nucleic acid based testing in Oncology
Molecular Diagnosis Nucleic acid based testing in Oncology Objectives Describe uses of NAT in Oncology Diagnosis, Prediction, monitoring. Genetics Screening, presymptomatic testing, diagnostic testing,
More informationNucleic Acid Testing - Oncology. Molecular Diagnosis. Gain/Loss of Nucleic Acid. Objectives. MYCN and Neuroblastoma. Molecular Diagnosis
Nucleic Acid Testing - Oncology Molecular Diagnosis Nucleic acid based testing in Oncology Gross alterations in DNA content of tumors (ploidy) Gain/Loss of nucleic acids Markers of Clonality Oncogene/Tumor
More informationChapter 18. mirna Expression Profiling: From Reference Genes to Global Mean Normalization
Chapter 18 mirna Expression Profiling: From Reference Genes to Global Mean Normalization Barbara D haene, Pieter Mestdagh, Jan Hellemans, and Jo Vandesompele Abstract MicroRNAs (mirnas) are an important
More informationSupplementary Information Titles Journal: Nature Medicine
Supplementary Information Titles Journal: Nature Medicine Article Title: Corresponding Author: Supplementary Item & Number Supplementary Fig.1 Fig.2 Fig.3 Fig.4 Fig.5 Fig.6 Fig.7 Fig.8 Fig.9 Fig. Fig.11
More informationThe Biology and Genetics of Cells and Organisms The Biology of Cancer
The Biology and Genetics of Cells and Organisms The Biology of Cancer Mendel and Genetics How many distinct genes are present in the genomes of mammals? - 21,000 for human. - Genetic information is carried
More informationmir 375 inhibits the proliferation of gastric cancer cells by repressing ERBB2 expression
EXPERIMENTAL AND THERAPEUTIC MEDICINE 7: 1757-1761, 2014 mir 375 inhibits the proliferation of gastric cancer cells by repressing ERBB2 expression ZHI YONG SHEN *, ZI ZHEN ZHANG *, HUA LIU, EN HAO ZHAO
More informationSupplementary information
Supplementary information Human Cytomegalovirus MicroRNA mir-us4-1 Inhibits CD8 + T Cell Response by Targeting ERAP1 Sungchul Kim, Sanghyun Lee, Jinwook Shin, Youngkyun Kim, Irini Evnouchidou, Donghyun
More informationIntroduction to Cancer Biology
Introduction to Cancer Biology Robin Hesketh Multiple choice questions (choose the one correct answer from the five choices) Which ONE of the following is a tumour suppressor? a. AKT b. APC c. BCL2 d.
More informationComputer Science, Biology, and Biomedical Informatics (CoSBBI) Outline. Molecular Biology of Cancer AND. Goals/Expectations. David Boone 7/1/2015
Goals/Expectations Computer Science, Biology, and Biomedical (CoSBBI) We want to excite you about the world of computer science, biology, and biomedical informatics. Experience what it is like to be a
More informationMicroRNAs: Regulatory Function and Potential for Gene Therapy
Lidia Park Genomics and Medicine November 23, 2008 MicroRNAs: Regulatory Function and Potential for Gene Therapy When Victor Ambros, Rosalind Lee, and Rhonda Feinbaum published the first finding of a microrna,
More informationEvidence for dietary regulation of microrna expression in cancer cells
Emerging Science Evidence for dietary regulation of microrna expression in cancer cells Cindy D Davis and Sharon A Ross MicroRNAs (mirnas) are an abundant class of short noncoding RNAs that are widely
More informationSupplementary Materials for
www.sciencesignaling.org/cgi/content/full/2/1/ra81/dc1 Supplementary Materials for Delivery of MicroRNA-126 by Apoptotic Bodies Induces CXCL12- Dependent Vascular Protection Alma Zernecke,* Kiril Bidzhekov,
More informationAn Epstein-Barr virus-encoded microrna targets PUMA to promote host cell survival
An Epstein-Barr virus-encoded microrna targets to promote host cell survival The Journal of Experimental Medicine 205(11): 2551-2560, 2008. 1 Elizabeth Yee-Wai Choy, Kam-Leung Siu, Kin-Hang Kok, Raymond
More informationmicrorna-449a functions as a tumor suppressor in neuroblastoma through inducing cell differentiation and cell cycle arrest
RNA Biology ISSN: 1547-6286 (Print) 1555-8584 (Online) Journal homepage: https://www.tandfonline.com/loi/krnb20 microrna-449a functions as a tumor suppressor in neuroblastoma through inducing cell differentiation
More informationMicroRNAs and Cancer
MicroRNAs and Cancer MicroRNAs are an abundant class of small (20-25 nucleotides) non-protein coding RNAs that function as negative gene regulators. The human genome contains up to 1000 micrornas which
More informationPREPARED FOR: U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland
AD Award Number: W81XWH-05-1-0471 TITLE: Dysregulation of RNA Interference in Breast Cancer PRINCIPAL INVESTIGATOR: Yin-Yuan Mo, Ph.D. CONTRACTING ORGANIZATION: Southern Illinois University Springfield,
More informationJ Clin Oncol 29: by American Society of Clinical Oncology INTRODUCTION
VOLUME 29 NUMBER 33 NOVEMBER 11 JOURNAL OF CLINICAL ONCOLOGY O R I G I N A L R E P O R T Prognostic Value of the Stage 4S Metastatic Pattern and Tumor Biology in Patients With Metastatic Neuroblastoma
More informationThe clinical relevance of circulating, cell-free and exosomal micrornas as biomarkers for gynecological tumors
Department of Tumor Biology The clinical relevance of circulating, cell-free and exosomal micrornas as biomarkers for gynecological tumors cfdna Copenhagen April 6-7, 2017 Heidi Schwarzenbach, PhD Tumor
More informationSupplementary Material
Supplementary Material Summary: The supplementary information includes 1 table (Table S1) and 4 figures (Figure S1 to S4). Supplementary Figure Legends Figure S1 RTL-bearing nude mouse model. (A) Tumor
More informationMicroRNA in Cancer Karen Dybkær 2013
MicroRNA in Cancer Karen Dybkær RNA Ribonucleic acid Types -Coding: messenger RNA (mrna) coding for proteins -Non-coding regulating protein formation Ribosomal RNA (rrna) Transfer RNA (trna) Small nuclear
More informationDetection of let-7a MicroRNA by Real-time PCR in Colorectal Cancer: a Single-centre Experience from China
The Journal of International Medical Research 2007; 35: 716 723 Detection of let-7a MicroRNA by Real-time PCR in Colorectal Cancer: a Single-centre Experience from China W-J FANG 1, C-Z LIN 2, H-H ZHANG
More informationHIF-inducible mir-191 promotes migration in breast cancer through complex regulation of TGFβ-signaling in hypoxic microenvironment.
HIF-inducible mir-9 promotes migration in breast cancer through complex regulation of TGFβ-signaling in hypoxic microenvironment. Neha Nagpal, Hafiz M Ahmad, Shibu Chameettachal3, Durai Sundar, Sourabh
More informationThe detection of differentially expressed micrornas from the serum of ovarian cancer patients using a novel real-time PCR platform
Available online at www.sciencedirect.com Gynecologic Oncology 112 (2009) 55 59 www.elsevier.com/locate/ygyno The detection of differentially expressed micrornas from the serum of ovarian cancer patients
More informationChapter 2. Investigation into mir-346 Regulation of the nachr α5 Subunit
15 Chapter 2 Investigation into mir-346 Regulation of the nachr α5 Subunit MicroRNA s (mirnas) are small (< 25 base pairs), single stranded, non-coding RNAs that regulate gene expression at the post transcriptional
More informationGenerating Spontaneous Copy Number Variants (CNVs) Jennifer Freeman Assistant Professor of Toxicology School of Health Sciences Purdue University
Role of Chemical lexposure in Generating Spontaneous Copy Number Variants (CNVs) Jennifer Freeman Assistant Professor of Toxicology School of Health Sciences Purdue University CNV Discovery Reference Genetic
More informationWhat causes cancer? Physical factors (radiation, ionization) Chemical factors (carcinogens) Biological factors (virus, bacteria, parasite)
Oncogenes What causes cancer? Chemical factors (carcinogens) Physical factors (radiation, ionization) Biological factors (virus, bacteria, parasite) DNA Mutation or damage Oncogenes Tumor suppressor genes
More informationFrom reference genes to global mean normalization
From reference genes to global mean normalization Jo Vandesompele professor, Ghent University co-founder and CEO, Biogazelle qpcr Symposium USA November 9, 2009 Millbrae, CA outline what is normalization
More informationIntroduction to Genetics
Introduction to Genetics Table of contents Chromosome DNA Protein synthesis Mutation Genetic disorder Relationship between genes and cancer Genetic testing Technical concern 2 All living organisms consist
More informationNature Genetics: doi: /ng Supplementary Figure 1. Phenotypic characterization of MES- and ADRN-type cells.
Supplementary Figure 1 Phenotypic characterization of MES- and ADRN-type cells. (a) Bright-field images showing cellular morphology of MES-type (691-MES, 700-MES, 717-MES) and ADRN-type (691-ADRN, 700-
More informationMolecular Hematopathology Leukemias I. January 14, 2005
Molecular Hematopathology Leukemias I January 14, 2005 Chronic Myelogenous Leukemia Diagnosis requires presence of Philadelphia chromosome t(9;22)(q34;q11) translocation BCR-ABL is the result BCR on chr
More informationSUPPLEMENTARY INFORMATION
DOI: 10.1038/ncb2607 Figure S1 Elf5 loss promotes EMT in mammary epithelium while Elf5 overexpression inhibits TGFβ induced EMT. (a, c) Different confocal slices through the Z stack image. (b, d) 3D rendering
More informationPublished Ahead of Print on October 3, 2011 as /JCO J Clin Oncol by American Society of Clinical Oncology INTRODUCTION
Published Ahead of Print on October 3, 11 as 10.10/JCO.11.35.9570 The latest version is at http://jco.ascopubs.org/cgi/doi/10.10/jco.11.35.9570 JOURNAL OF CLINICAL ONCOLOGY O R I G I N A L R E P O R T
More informationMicroRNA-92gene expression in epithelial ovarian cancer using a novel Real-Time Polymerase change reaction
www.muthjm.com Muthanna Medical Journal 2016; 3(1):23-33 MicroRNA-92gene expression in epithelial ovarian cancer using a novel Real-Time Polymerase change reaction Shoroq Mohammed AL-Temimi 1* Abstract
More informationThe functional investigation of the interaction between TATA-associated factor 3 (TAF3) and p53 protein
THESIS BOOK The functional investigation of the interaction between TATA-associated factor 3 (TAF3) and p53 protein Orsolya Buzás-Bereczki Supervisors: Dr. Éva Bálint Dr. Imre Miklós Boros University of
More informationSupplementary Figure 1 Transcription assay of nine ABA-responsive PP2C. Transcription assay of nine ABA-responsive PP2C genes. Total RNA was isolated
Supplementary Figure 1 Transcription assay of nine ABA-responsive PP2C genes. Transcription assay of nine ABA-responsive PP2C genes. Total RNA was isolated from 7 day-old seedlings treated with or without
More informationThe Putative Tumor Suppressor microrna-101 Modulates the Cancer Epigenome by Repressing the Polycomb Group Protein EZH2
Published Online First on March 3, 2009 as 10.1158/0008-5472.CAN-08-3114 The Putative Tumor Suppressor microrna-101 Modulates the Cancer Epigenome by Repressing the Polycomb Group Protein EZH2 Jeffrey
More informationSupplementary Fig. 1. Delivery of mirnas via Red Fluorescent Protein.
prfp-vector RFP Exon1 Intron RFP Exon2 prfp-mir-124 mir-93/124 RFP Exon1 Intron RFP Exon2 Untransfected prfp-vector prfp-mir-93 prfp-mir-124 Supplementary Fig. 1. Delivery of mirnas via Red Fluorescent
More informationVariations in Chromosome Structure & Function. Ch. 8
Variations in Chromosome Structure & Function Ch. 8 1 INTRODUCTION! Genetic variation refers to differences between members of the same species or those of different species Allelic variations are due
More informationMolecular Markers. Marcie Riches, MD, MS Associate Professor University of North Carolina Scientific Director, Infection and Immune Reconstitution WC
Molecular Markers Marcie Riches, MD, MS Associate Professor University of North Carolina Scientific Director, Infection and Immune Reconstitution WC Overview Testing methods Rationale for molecular testing
More informationSUPPLEMENTARY FIGURE LEGENDS
SUPPLEMENTARY FIGURE LEGENDS Supplementary Figure 1 Negative correlation between mir-375 and its predicted target genes, as demonstrated by gene set enrichment analysis (GSEA). 1 The correlation between
More informationTITLE: Identifying that Regulate Neuroblastoma Cell Differentiation
Award Number: W81XWH-13-1-0241 TITLE: Identifying that Regulate Neuroblastoma Cell Differentiation PRINCIPAL INVESTIGATOR: Dr. Liqin Du CONTRACTING ORGANIZATION: University of Texas Health Science Center
More informationSupplementary Information. Induction of p53-independent apoptosis by ectopic expression of HOXA5
Supplementary Information Induction of p53-independent apoptosis by ectopic expression of in human liposarcomas Dhong Hyun Lee 1, *, Charles Forscher 1, Dolores Di Vizio 2, 3, and H. Phillip Koeffler 1,
More informationLing Xu, Wei-Qi Dai, Xuan-Fu Xu, Fan Wang, Lei He, Chuan-Yong Guo*
DOI:http://dx.doi.org/10.7314/APJCP.2012.13.7.3203 RESEARCH ARTICLE Effects of Multiple-target Anti-microRNA Antisense Oligodeoxyribonucleotides on Proliferation and Migration of Gastric Cancer Cells Ling
More informationType of file: PDF Size of file: 0 KB Title of file for HTML: Supplementary Information Description: Supplementary Figures
Type of file: PDF Size of file: 0 KB Title of file for HTML: Supplementary Information Description: Supplementary Figures Supplementary Figure 1 mir-128-3p is highly expressed in chemoresistant, metastatic
More informationp.r623c p.p976l p.d2847fs p.t2671 p.d2847fs p.r2922w p.r2370h p.c1201y p.a868v p.s952* RING_C BP PHD Cbp HAT_KAT11
ARID2 p.r623c KMT2D p.v650fs p.p976l p.r2922w p.l1212r p.d1400h DNA binding RFX DNA binding Zinc finger KMT2C p.a51s p.d372v p.c1103* p.d2847fs p.t2671 p.d2847fs p.r4586h PHD/ RING DHHC/ PHD PHD FYR N
More informationMicroRNA-mediated incoherent feedforward motifs are robust
The Second International Symposium on Optimization and Systems Biology (OSB 8) Lijiang, China, October 31 November 3, 8 Copyright 8 ORSC & APORC, pp. 62 67 MicroRNA-mediated incoherent feedforward motifs
More informationSupplementary Information. Preferential associations between co-regulated genes reveal a. transcriptional interactome in erythroid cells
Supplementary Information Preferential associations between co-regulated genes reveal a transcriptional interactome in erythroid cells Stefan Schoenfelder, * Tom Sexton, * Lyubomira Chakalova, * Nathan
More informationHALLA KABAT * Outreach Program, mircore, 2929 Plymouth Rd. Ann Arbor, MI 48105, USA LEO TUNKLE *
CERNA SEARCH METHOD IDENTIFIED A MET-ACTIVATED SUBGROUP AMONG EGFR DNA AMPLIFIED LUNG ADENOCARCINOMA PATIENTS HALLA KABAT * Outreach Program, mircore, 2929 Plymouth Rd. Ann Arbor, MI 48105, USA Email:
More informationProblem Set 8 Key 1 of 8
7.06 2003 Problem Set 8 Key 1 of 8 7.06 2003 Problem Set 8 Key 1. As a bright MD/PhD, you are interested in questions about the control of cell number in the body. Recently, you've seen three patients
More informationSmall RNAs and how to analyze them using sequencing
Small RNAs and how to analyze them using sequencing Jakub Orzechowski Westholm (1) Long- term bioinforma=cs support, Science For Life Laboratory Stockholm (2) Department of Biophysics and Biochemistry,
More informationCombined transfection of Bcl-2 sirna and mir-15a oligonucleotides enhanced methotrexate-induced apoptosis in Raji cells
Cancer Biol Med 2013;10:16-21. doi: 10.7497/j.issn.2095-3941.2013.01.003 ORIGINAL ARTICLE Combined transfection of Bcl-2 sirna and mir-15a oligonucleotides enhanced methotrexate-induced apoptosis in Raji
More informationDOES THE BRCAX GENE EXIST? FUTURE OUTLOOK
CHAPTER 6 DOES THE BRCAX GENE EXIST? FUTURE OUTLOOK Genetic research aimed at the identification of new breast cancer susceptibility genes is at an interesting crossroad. On the one hand, the existence
More informationEpstein-Barr virus driven promoter hypermethylated genes in gastric cancer
RESEARCH FUND FOR THE CONTROL OF INFECTIOUS DISEASES Epstein-Barr virus driven promoter hypermethylated genes in gastric cancer J Yu *, KF To, QY Liang K e y M e s s a g e s 1. Somatostatin receptor 1
More informationCONTRACTING ORGANIZATION: Rutgers University Piscataway, NJ
AD Award Number: W81XWH-05-1-0483 TITLE: Role of microrna Genes in Breast Cancer Progression PRINCIPAL INVESTIGATOR: Richard W. Padgett, Ph.D. CONTRACTING ORGANIZATION: Rutgers University Piscataway, NJ
More informationDownregulation of serum mir-17 and mir-106b levels in gastric cancer and benign gastric diseases
Brief Communication Downregulation of serum mir-17 and mir-106b levels in gastric cancer and benign gastric diseases Qinghai Zeng 1 *, Cuihong Jin 2 *, Wenhang Chen 2, Fang Xia 3, Qi Wang 3, Fan Fan 4,
More informationIs Multiplex Ligation-dependent Probe Amplification a good method for screening formalin fixed paraffin embedded neuroblastoma tumors?
Is Multiplex Ligation-dependent Probe Amplification a good method for screening formalin fixed paraffin embedded neuroblastoma tumors? Bachelor Degree Project in Biomedicine (2011-03-28 2012-01-11) 30
More informationPolyomaviridae. Spring
Polyomaviridae Spring 2002 331 Antibody Prevalence for BK & JC Viruses Spring 2002 332 Polyoma Viruses General characteristics Papovaviridae: PA - papilloma; PO - polyoma; VA - vacuolating agent a. 45nm
More informationIdentification of a MicroRNA Panel for Clear-cell Kidney Cancer
Identification of a MicroRNA Panel for Clear-cell Kidney Cancer Cancer David Juan, Gabriela Alexe, Travis Antes, Huiqing Liu, Anant Madabhushi, Charles Delisi, Shridhar Ganesan, Gyan Bhanot, and Louis
More informationAssociation of mir-21 with esophageal cancer prognosis: a meta-analysis
Association of mir-21 with esophageal cancer prognosis: a meta-analysis S.-W. Wen 1, Y.-F. Zhang 1, Y. Li 1, Z.-X. Liu 2, H.-L. Lv 1, Z.-H. Li 1, Y.-Z. Xu 1, Y.-G. Zhu 1 and Z.-Q. Tian 1 1 Department of
More information(A) Cells grown in monolayer were fixed and stained for surfactant protein-c (SPC,
Supplemental Figure Legends Figure S1. Cell line characterization (A) Cells grown in monolayer were fixed and stained for surfactant protein-c (SPC, green) and co-stained with DAPI to visualize the nuclei.
More informationSupplementary Table 2: ALK mutations in neuroblastoma cell lines and comparison
Supplementary data Supplementary Table 2: ALK mutations in neuroblastoma cell lines and comparison with published studies. (MNA = MYCN amplification, A = MYCN amplified, NA = not MYCN amplified, wt = wild-type).
More informationNeurotrophic factor GDNF and camp suppress glucocorticoid-inducible PNMT expression in a mouse pheochromocytoma model.
161 Neurotrophic factor GDNF and camp suppress glucocorticoid-inducible PNMT expression in a mouse pheochromocytoma model. Marian J. Evinger a, James F. Powers b and Arthur S. Tischler b a. Department
More informationhe micrornas of Caenorhabditis elegans (Lim et al. Genes & Development 2003)
MicroRNAs: Genomics, Biogenesis, Mechanism, and Function (D. Bartel Cell 2004) he micrornas of Caenorhabditis elegans (Lim et al. Genes & Development 2003) Vertebrate MicroRNA Genes (Lim et al. Science
More informationoncogenes-and- tumour-suppressor-genes)
Special topics in tumor biochemistry oncogenes-and- tumour-suppressor-genes) Speaker: Prof. Jiunn-Jye Chuu E-Mail: jjchuu@mail.stust.edu.tw Genetic Basis of Cancer Cancer-causing mutations Disease of aging
More informationDoctoral Degree Program in Marine Biotechnology, College of Marine Sciences, Doctoral Degree Program in Marine Biotechnology, Academia Sinica, Taipei,
Cyclooxygenase 2 facilitates dengue virus replication and serves as a potential target for developing antiviral agents Chun-Kuang Lin 1,2, Chin-Kai Tseng 3,4, Yu-Hsuan Wu 3,4, Chih-Chuang Liaw 1,5, Chun-
More informationmir-16 promotes the apoptosis of human cancer cells by targeting FEAT
Liang et al. BMC Cancer (2015) 15:448 DOI 10.1186/s12885-015-1458-8 RESEARCH ARTICLE Open Access mir-16 promotes the apoptosis of human cancer cells by targeting FEAT Hongwei Liang 2,ZhengFu 2, Xueyuan
More informationDeciphering the Role of micrornas in BRD4-NUT Fusion Gene Induced NUT Midline Carcinoma
www.bioinformation.net Volume 13(6) Hypothesis Deciphering the Role of micrornas in BRD4-NUT Fusion Gene Induced NUT Midline Carcinoma Ekta Pathak 1, Bhavya 1, Divya Mishra 1, Neelam Atri 1, 2, Rajeev
More information