PRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative stress
- Authors:
- Published online on: July 21, 2016 https://doi.org/10.3892/ol.2016.4899
- Pages: 2217-2221
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
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 (H2O2)‑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 H2O2‑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 H2O2. 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.
