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Aberrant Regulation of HDAC2 Mediates Proliferation of Hepatocellular Carcinoma Cells by Deregulating Expression of G1/S Cell Cycle Proteins

ABSTRACT: To investigate the specific roles of HDAC2 in the development of liver cancer, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the Hep3B cells transfected with HDAC2 shRNAs, and recapitulated molecular signatures that related to hallmarks of cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32070 | GEO | 2012/03/01

SECONDARY ACCESSION(S): PRJNA147593

REPOSITORIES: GEO

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Aberrant Regulation of HDAC2 Mediates Proliferation of Hepatocellular Carcinoma Cells by Deregulating Expression of G1/S Cell Cycle Proteins

Project description:To investigate the specific roles of HDAC2 in the development of liver cancer, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the Hep3B cells transfected with HDAC2 shRNAs, and recapitulated molecular signatures that related to hallmarks of cancer. With the aim of identifying changes in gene expression following gene knockdown of HDAC2, we performed expression profiling in shRNA expression vector-transfected Hep3B cells, and compared the results to those obtained from vector-transfected Hep3B cells.

2012-03-01 | E-GEOD-32070 | biostudies-arrayexpress

HDAC2 Mediates Gene Inactivating of p16INK4a and Promotes Gastric Carcinogenesis by Enhancing Cell Survival and Growth

Project description:To investigate the specific roles of HDAC2 in the development of gastric cancer, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the MKN-1 cells transfected with HDAC2 shRNAs, and recapitulated molecular signatures that related to hallmarks of cancer. DNA methylation of p16INK4a promoter region was assessed by methylation specific polymerase chain reaction. Recruiting the HDAC2 at the p16INK4a promoter was identified using chromatin immunoprecipitation assay. RNA interference-mediated protein knockdown method was used to investigate oncogenic potential of HDAC2 in in vitro and in vivo gastrocarcinogenesis of MKN-1 cells. RNA interference-mediated protein knockdown versus mock treatment

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Project description:To investigate the specific roles of SIRT7 in the development of HCC, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the Hep3B cells transfected with SIRT7 shRNAs, and recapitulated molecular signatures that related to hallmarks of cancer.

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Aberrant regulation of HDAC2 mediates proliferation of hepatocellular carcinoma cells by deregulating expression of G1/S cell cycle proteins.

Project description: Not available

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HDAC6 functions as a tumor suppressor by activating caspase-independent autophagic cell death in hepatocarcinogenesis

Project description:To investigate the specific roles of HDAC6 in the development of liver cancer, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the Hep3B cells transfected with empty mock or pcDNA_HDAC6, and recapitulated molecular signatures that related to hallmarks of cancer. To characterize the biological effects of HDAC6 on liver cancer, large-scale gene expression analysis to identify molecular signature was performed on the Hep3B cells.

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Primary human erythroid progenitor cells HDAC1 and HDAC2 shRNA knockdown samples

Project description:Gene expression profiling was performed on primary human erythroid progenitor cells expressing a control shRNA (luciferase), two different HDAC1 shRNAs, and two different HDAC2 shRNAs. The worldwide burden of sickle cell disease is enormous, with over 200,000 infants born with the disease each year in Africa alone. Induction of fetal hemoglobin is a validated strategy to improve symptoms and complications of this disease. The development of targeted therapies has been limited by the absence of discrete druggable targets. We developed a novel bead-based strategy for the identification of inducers of fetal hemoglobin transcripts in primary human erythroid cells. A small-molecule screen of bioactive compounds identified remarkable class-associated activity among histone deacetylase (HDAC) inhibitors. Using a chemical genetic strategy combining focused libraries of biased chemical probes and reverse genetics by RNA interference, we have identified HDAC1 and HDAC2 as molecular targets mediating fetal hemoglobin induction. Our findings suggest the potential of isoform-selective inhibitors of HDAC1 and HDAC2 for the treatment of sickle cell disease. Gene expression profiling was performed on primary human erythroid progenitor cells expressing a control shRNA (luciferase, n=3), two different HDAC1 shRNAs (n=2 and n=3), and two different HDAC2 shRNAs (n=3 for each).

2010-07-29 | E-GEOD-22366 | biostudies-arrayexpress

HDAC6 functions as a tumor suppressor by activating caspase-independent autophagic cell death in hepatocarcinogenesis

2012-03-01 | GSE32068 | GEO

Primary human erythroid progenitor cells HDAC1 and HDAC2 shRNA knockdown samples

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Role of Hdac2 in pancreatic ductal adenocarcinoma

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