Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA175703 | ENA |
REPOSITORIES: ENA
Similar Datasets
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 miRNA expression analysis using Immunopreticipated RNA fractions with anti-human-Argonute 2 antibody for non-treated, miR-195 or miR-497 overexpressed Hep G2 cell.
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.
2013-05-31 | E-GEOD-41074 | 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. 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.
2013-05-31 | GSE41074 | 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. Screening of frequently downregulated miRNAs by comparing endgeneous expression status of miRNAs in 6 HCC cell lines with 2 normal livers Expression analysis using total RNAs extracted from standard medium conditioned 6 HCC cell lines, and 2 normal livers derived from patients with hepatectomy due to metastatic liver tumor
2013-05-31 | E-GEOD-41077 | 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. Screening of frequently downregulated miRNAs by comparing endgeneous expression status of miRNAs in 6 HCC cell lines with 2 normal livers
2013-05-31 | GSE41077 | GEO
Project description:The aim of the study is to identify miRNA specific targets in Hodgkin lymphoma cell lines. By immunoprecipitation (IP) of wild type Ago2, Ago2 associated gene transcripts (ie miRNA targets) are coimmunoprecipitated. In cells transfected with anti-miR-17/20/93/106, the miR-17 seed family specific targets are not coimmunoprecipitated with Ago2. With microarray analysis, signal intensities of probes associated with Ago2 from untransfected and anti-miRNA transfected cells are compared. Gene transcripts that are depleted from the Ago2-IP fraction upon miRNA inhibition (ie miRNA specific targets) are identified.
2009-10-13 | GSE16053 | GEO
Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Argonaute 2 (Ago2)-immunoprecipitation (IP) after miR-195 or miR-497 overexpression in HepG2
| PRJNA175701 | ENA
Project description:Despite considerable improvements in the treatment of B-cell precursor acute lymphoblastic leukemia (BCP-ALL), relapse is still associated with poor prognosis. We previously found that the risk for early relapse can be predicted by the rapid engraftment of patient-derived blasts transplanted into NOD/SCID mice. In search for the cellular and molecular profile associated with this phenotype, we investigated the expression of microRNAs (miRNAs) in different engraftment phenotypes and patient outcomes. We found miR-497~195 high expression in patient-derived xenograft samples with slow engraftment, derived from patients with favorable outcome. In contrast, epigenetic repression and low expression of these miRNAs was observed in rapidly engrafting samples, which were associated with early relapse. Overexpression of miR-497~195 in patient-derived cells suppressed in vivo engraftment of leukemia cells and considerably prolonged recipient survival by inhibition of regulators of cell cycle progression. As key factors for the entry in S phase were downregulated upon miR-497~195 overexpression, we identified CDK4/CCND3 mediated control of G1/S transition as a principal mechanism for miR-497~195 mediated suppression of leukemia progression in BCP-ALL. Thus, the association of the miR-497~195 cluster expression with outcome in BCP-ALL, and the importance of these miRNAs in counteracting the development of ALL in vivo indicate the relevance of the involved pathways as potential targets for therapeutic intervention.
2022-12-09 | GSE141779 | GEO
Project description:Despite considerable improvements in the treatment of B-cell precursor acute lymphoblastic leukemia (BCP-ALL), relapse is still associated with poor prognosis. We previously found that the risk for early relapse can be predicted by the rapid engraftment of patient-derived blasts transplanted into NOD/SCID mice. In search for the cellular and molecular profile associated with this phenotype, we investigated the expression of microRNAs (miRNAs) in different engraftment phenotypes and patient outcomes. We found miR-497~195 high expression in patient-derived xenograft samples with slow engraftment, derived from patients with favorable outcome. In contrast, epigenetic repression and low expression of these miRNAs was observed in rapidly engrafting samples, which were associated with early relapse. Overexpression of miR-497~195 in patient-derived cells suppressed in vivo engraftment of leukemia cells and considerably prolonged recipient survival by inhibition of regulators of cell cycle progression. As key factors for the entry in S phase were downregulated upon miR-497~195 overexpression, we identified CDK4/CCND3 mediated control of G1/S transition as a principal mechanism for miR-497~195 mediated suppression of leukemia progression in BCP-ALL. Thus, the association of the miR-497~195 cluster expression with outcome in BCP-ALL, and the importance of these miRNAs in counteracting the development of ALL in vivo indicate the relevance of the involved pathways as potential targets for therapeutic intervention.
2022-12-09 | GSE141774 | GEO