Open AccessSIRT1 promotes tumorigenesis of hepatocellular carcinoma through PI3K/PTEN/AKT signaling
Author(s) -
Hanning Wang,
Hao Liu,
Kaiyun Chen,
Jinfeng Xiao,
Ke He,
Jinqian Zhang,
Guoan Xiang
Publication year - 2012
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2012.1788
Subject(s) - pten , carcinogenesis , pi3k/akt/mtor pathway , cancer research , biology , protein kinase b , apoptosis , cell cycle , oncogene , cell growth , liver cancer , signal transduction , microbiology and biotechnology , cancer , hepatocellular carcinoma , biochemistry , genetics
SIRT1 is the human orthologue of SIR2, a conserved NAD-dependent proteindeacetylase that regulates longevity in yeast and in Caenorhabditis elegans. Overexpressionof SIRT1 in cancer tissue, compared with normal tissue, has been demonstrated,suggesting that SIRT1 may act as a tumor promoter. The function of SIRT1 in livercancer has not been elucidated. In the present study, SIRT1 re-expression or knockdownwas induced in hepatoma cell lines and liver normal cell lines. Our study demonstratedthat overexpression of SIRT1 promoted mitotic entry of liver cells, cell growthand proliferation and inhibited apoptosis. The apoptosis involved caspase-3 andcaspase-7, and was related to the PTEN/PI3K/AKT signaling pathway. The resultsdemonstrate that SIRT1 promotes tumorigenesis of hepatocellular carcinoma (HCC)through the PTEN/PI3K/AKT signaling pathway. SIRT1 may serve as a novel targetfor selective killing of cancer versus normal liver cells.
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