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10.3892/ol.2016.4899 http://scihub22266oqcxt.onion/10.3892/ol.2016.4899 C4998565!4998565!27602166     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncol+Lett 2016 ; 12 (3): 2217-21 Nephropedia Template TP {{tp|p=27602166|t=2016. PRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative stress |pdf=|usr=}}{{27602166}} gab.com Text PRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative stress JO: Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=27602166 #FOAvip 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-? (TNF-?)-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-?-induced apoptosis, whereas PRDX2 overexpression reduced it, even though both treatments showed little effects on TNF-?-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. Twit Text FOAVip PRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative stress ????Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=27602166 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27602166 #FOAvip English Wikipedia <ref>{{Cite pmid|27602166}}</ref> PRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative stress #MMPMID27602166 Zhou S; Han Q; Wang R; Li X; Wang Q; Wang H; Wang J; Ma Y Oncol Lett 2016[Sep]; 12 (3): 2217-21 PMID27602166show ga 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-? (TNF-?)-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-?-induced apoptosis, whereas PRDX2 overexpression reduced it, even though both treatments showed little effects on TNF-?-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. äPRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative(epmc).pdf DeepDyve Pubget Overpricing