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GEO help: Mouse over screen elements for information. |
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Status |
Public on Aug 17, 2011 |
Title |
HDAC2 Mediates Gene Inactivating of p16INK4a and Promotes Gastric Carcinogenesis by Enhancing Cell Survival and Growth |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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Summary |
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.
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Overall design |
RNA interference-mediated protein knockdown versus mock treatment
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Contributor(s) |
Kim J, Noh J, Eun J, Jung K, Bae H, Xie H, Kim M, Chang Y, Park W, Lee J, Nam S |
Citation(s) |
23175521, 24448241 |
Submission date |
Aug 11, 2011 |
Last update date |
Oct 18, 2022 |
Contact name |
Jung Woo Eun |
E-mail(s) |
jetaimebin@catholic.ac.kr
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Organization name |
Ajou University of Korea
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Street address |
Department of Gastroenterology
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City |
Suwon, Korea |
State/province |
Korea |
ZIP/Postal code |
16499 |
Country |
South Korea |
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Platforms (1) |
GPL10558 |
Illumina HumanHT-12 V4.0 expression beadchip |
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Samples (2) |
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Relations |
BioProject |
PRJNA145919 |
Supplementary file |
Size |
Download |
File type/resource |
GSE31338_RAW.tar |
26.2 Mb |
(http)(custom) |
TAR |
GSE31338_non-normalized.txt.gz |
790.2 Kb |
(ftp)(http) |
TXT |
Processed data included within Sample table |
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