Unknown,Transcriptomics,Genomics,Proteomics

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Differential gene expression of the human colon carcinoma cell line HCT-116 upon Entinostat treatment

ABSTRACT: Class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with HDAC inhibitors (such as Entinostat) as well as the specific genetic elimination of HDAC1 and HDAC2 leads to a reduced expression of p53 mRNA levels and a subsequent depletion of mutant p53 protein expression. To investigate other tumor entities we also tested the human colon carcinoma cell line HCT-116, which was treated for 24h with 2ÂµM Entinostat or treated with vehicle control. Total mRNA was isolated and checked for integrity. According to manufacture's recommendation the samples were subjected to microarray analysis using the Affymetrix Human Gene ST 2.0 array chip to discover differentially expressed genes.

ORGANISM(S): Homo sapiens

SUBMITTER: Matthias Wirth

PROVIDER: E-MTAB-4303 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Histone deacetylases (Hdac) remove acetyl groups from proteins, influencing global and specific gene expression. Hdacs control inflammation, as shown by Hdac inhibitor-dependent protection from DSS-induced murine colitis. While tissue-specific Hdac knockouts show redundant and specific functions, little is known of their intestinal epithelial cell (IEC) role. We have shown previously that dual Hdac1/Hdac2 IEC-specific loss disrupts cell proliferation and determination, with decreased secretory cell numbers and altered barrier function. We thus investigated how compound Hdac1/Hdac2 or Hdac2 IEC-specific deficiency alters the inflammatory response. Floxed Hdac1 and Hdac2 and villin-Cre mice were interbred. Compound Hdac1/Hdac2 IEC-deficient mice showed chronic basal inflammation, with increased basal Disease Activity Index (DAI) and deregulated Reg gene colonic expression. DSS-treated dual Hdac1/Hdac2 IEC-deficient mice displayed increased DAI, histological score, intestinal permeability and inflammatory gene expression. In contrast to double knockouts, Hdac2 IEC-specific loss did not affect IEC determination and growth, nor result in chronic inflammation. However, Hdac2 disruption protected against DSS colitis, as shown by decreased DAI, intestinal permeability and caspase-3 cleavage. Hdac2 IEC-specific deficient mice displayed increased expression of IEC gene subsets, such as colonic antimicrobial Reg3b and Reg3g mRNAs, and decreased expression of immune cell function-related genes. Our data show that Hdac1 and Hdac2 are essential IEC homeostasis regulators. IEC-specific Hdac1 and Hdac2 may act as epigenetic sensors and transmitters of environmental cues and regulate IEC-mediated mucosal homeostatic and inflammatory responses. Different levels of IEC Hdac activity may lead to positive or negative outcomes on intestinal homeostasis during inflammation Total RNAs from the colon of three control and three Hdac2 IEC-specific knockout mice were isolated with the Rneasy kit (Qiagen, Mississauga, ON, Canada).

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Differential gene expression of the human colon carcinoma cell line HCT-116 upon Entinostat treatment

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