Open AccessPRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative stress
Author(s) -
Silei Zhou,
Qi Han,
Wang Ru,
Xin Li,
Qingyang Wang,
Huizhong Wang,
Jing Wang,
Yun Ma
Publication year - 2016
Publication title -
oncology letters
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.4899
Subject(s) - gene knockdown , oxidative stress , apoptosis , carcinogenesis , programmed cell death , cancer research , microbiology and biotechnology , chemistry , biology , cancer , biochemistry , genetics
Peroxiredoxin2 (PRDX2) is a member of the peroxiredoxin family of antioxidant enzymes. A number of previous studies have indicated that PRDX2 may serve a cell type-dependent role in tumorigenesis. Recently, PRDX2 has been identified to be the new target of miR-122a, which has been demonstrated to be frequently downregulated in hepatocellular carcinoma (HCC). Thus, PRDX2 may have a pro-tumorigenic role in HCC. Because the role of PRDX2 in HCC has not yet been reported, it is of interest to explore how PRDX2 may affect reactive oxygen species (ROS)-mediated cell death in HCC cells. The present study analyzed the effects of PRDX2 knockdown or overexpression on hydrogen peroxide (H 2 O 2 )-induced cell death in HCC SMMC-7721 cells. Tumor necrosis factor-α (TNF-α)-induced cell death upon PRDX2 knockdown or overexpression was also examined in SMMC-7721 cells. It was found that PRDX2 knockdown augmented H 2 O 2 -induced cell death in SMMC-7721 cells, whereas PRDX2 overexpression exhibited opposite effects. By contrast, PRDX2 knockdown enhanced TNF-α-induced apoptosis, whereas PRDX2 overexpression reduced it, even though both treatments showed little effects on TNF-α-induced necrosis in SMMC-7721 cells. Further exploration confirmed PRDX2 knockdown led to enhanced ROS generation in response to H 2 O 2 . Taken together, the present study supports that PRDX2 serves a pro-tumorigenic role in HCC through, at least partially, limiting ROS-mediated apoptosis under oxidative stress.