Analysis of expression profiles in miR-195 transduced Ebf1–/– Lin– cells
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PROVIDER: PRJNA1034100 | ENA |
REPOSITORIES: ENA
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Project description:To further investigate whether miR-195 transduction lead Ebf1–/– Lin– cells to develop into later stages than pro B, we have employed microarray expression profiling. For the purpose, we compared B cell and other lineages (T cell, NK cell and myeloid) related gene expressions among these samples.
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2016-08-23 | GSE85884 | GEO
Project description:miRNAs are related with the initiation and development of prostate cancer. We discover the miR-195 and miR-30 can be as a biomarker of prognosis of prostate cancer in clinical patients. miRNA functions through affecting the mRNA degradation by binding the mRNA 3âUTR. So we test the change of transcriptional profile of miR-195 and miR-30d cell line respectively to further study the function of miR-195 and miR-30d. To study the function of miR-195 and miR-30d in prostate cancer, we setup the over-expression cell line of the miR-195 and miR-30d respectively in prostate cancer cell(LNCap and DU145), then study the change of transcriptional profile in cell line by microarray experiment (Affymetrix PrimeView human gene expression). We order the over-expression plasmid of vector, miR-195 and miR-30d from System Biosciences company (Cat No: Scramble Vector PMIRH000PA-1 as Control, miR-195 PMIRH195PA-1, miR-30d PMIRH30dPA-1), and packaged the virus and construct the stable cell line (LNCaP_Control, LNCaP_mir195, LNCaP_mir30d,DU145_Control, DU145_mir195, DU145_mir30d,). We test the transcriptional profile in cell line by microarray experiment (Affymetrix PrimeView human gene expression).
2016-08-23 | E-GEOD-85884 | biostudies-arrayexpress
Project description:The experiment was designed to identify the genes which get altered after over-expression and depletion of hsa-miR-195 levels in MCF7 and HEK 293T cells. Recent research has established that microRNAs (miRNAs) are key regulators of many cell processes including those often deregulated in cancer such as apoptosis. In our previous work we have shown that hsa-miR-195 targets the key anti-apoptotic molecule BCL2 and its over-expression induces apoptosis and augments sensitivity of cancer cells towards chemotherapeutic drug. These results suggested a possible anticancer role of miR-195 and therefore oblige its complete functional characterization. In this study global effect of alterations in cellular miR-195 levels on transcriptome was analysed in order to identify the regulatory functions of miR-195. Together our findings highlight a novel and important role of hsa-miR-195 potentially opening new avenues for the treatment of various diseases.
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2013-05-31 | E-GEOD-41079 | biostudies-arrayexpress
Project description:To explore functionally crucial tumor-suppressive (TS)-miRNAs in hepatocellular carcinoma (HCC), we performed integrative function- and expression-based screenings of TS-miRNAs in six HCC cell lines. The screenings identified seven miRNAs, which showed growth-suppressive activities through the overexpression of each miRNA and were endogenously downregulated in HCC cell lines. Further expression analyses using a large panel of HCC cell lines and primary tumors demonstrated four miRNAs, miR-101, -195, -378 and -497, as candidate TS-miRNAs frequently silenced in HCCs. Among them, two clustered miRNAs miR-195 and miR-497 showed significant growth-suppressive activity with induction of G1 arrest. Comprehensive exploration of their targets using Argonute2-immunoprecipitation-deep-sequencing (Ago2-IP-seq) and genome-wide expression profiling after their overexpression, successfully identified a set of cell-cycle regulators, including CCNE1, CDC25A, CCND3, CDK4, and BTRC. Our results suggest the molecular pathway regulating cell cycle progression to be integrally altered by downregulation of miR-195 and miR-497 expression, leading to aberrant cell proliferation in hepatocarcinogenesis. Analysis of miRNA profile change in the Ago2-IP fraction after overexpression with miR-195 or miR-497
2013-05-31 | GSE41079 | GEO
Project description:To explore functionally crucial tumor-suppressive (TS)-miRNAs in hepatocellular carcinoma (HCC), we performed integrative function- and expression-based screenings of TS-miRNAs in six HCC cell lines. The screenings identified seven miRNAs, which showed growth-suppressive activities through the overexpression of each miRNA and were endogenously downregulated in HCC cell lines. Further expression analyses using a large panel of HCC cell lines and primary tumors demonstrated four miRNAs, miR-101, -195, -378 and -497, as candidate TS-miRNAs frequently silenced in HCCs. Among them, two clustered miRNAs miR-195 and miR-497 showed significant growth-suppressive activity with induction of G1 arrest. Comprehensive exploration of their targets using Argonute2-immunoprecipitation-deep-sequencing (Ago2-IP-seq) and genome-wide expression profiling after their overexpression, successfully identified a set of cell-cycle regulators, including CCNE1, CDC25A, CCND3, CDK4, and BTRC. Our results suggest the molecular pathway regulating cell cycle progression to be integrally altered by downregulation of miR-195 and miR-497 expression, leading to aberrant cell proliferation in hepatocarcinogenesis. Identification of miR-195 and miR-497 target genes by sequencing Ago2-binding mRNAs and total mRNAs of miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell. Deep sequencing of RNAs in Ago2-IP fraction and mRNAs extracted from miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell.
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