PMID- 27602166
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 12
IP  - 3
DP  - 2016 Sep
TI  - PRDX2 protects hepatocellular carcinoma SMMC-7721 cells from oxidative stress.
PG  - 2217-2221
AB  - 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-alpha 
      (TNF-alpha)-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-alpha-induced 
      apoptosis, whereas PRDX2 overexpression reduced it, even though both treatments 
      showed little effects on TNF-alpha-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.
FAU - Zhou, Silei
AU  - Zhou S
AD  - Key Laboratory of Cellular and Molecular Immunology, Henan University, Kaifeng, 
      Henan 475001, P.R. China; Department of Molecular Immunology, Institute of Basic 
      Medical Sciences, Beijing 100850, P.R. China.
FAU - Han, Quanli
AU  - Han Q
AD  - Department of Medical Oncology 2, Chinese PLA General Hospital & Chinese PLA 
      Medical Academy, Beijing 100853, P.R. China.
FAU - Wang, Ru
AU  - Wang R
AD  - Clinical Laboratory, 305 Hospital of PLA, Beijing 100017, P.R. China.
FAU - Li, Xin
AU  - Li X
AD  - Department of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 
      100850, P.R. China.
FAU - Wang, Qingyang
AU  - Wang Q
AD  - Department of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 
      100850, P.R. China.
FAU - Wang, Huizhong
AU  - Wang H
AD  - Clinical Laboratory, 305 Hospital of PLA, Beijing 100017, P.R. China.
FAU - Wang, Jing
AU  - Wang J
AD  - Department of Radiation Oncology, Chinese PLA General Hospital & Chinese PLA 
      Medical Academy, Beijing 100853, P.R. China.
FAU - Ma, Yuanfang
AU  - Ma Y
AD  - Key Laboratory of Cellular and Molecular Immunology, Henan University, Kaifeng, 
      Henan 475001, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20160721
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC4998565
OTO - NOTNLM
OT  - apoptosis
OT  - cell death
OT  - hepatocellular carcinoma
OT  - oxidative stress
OT  - peroxiredoxin 2
EDAT- 2016/09/08 06:00
MHDA- 2016/09/08 06:01
PMCR- 2016/07/21
CRDT- 2016/09/08 06:00
PHST- 2015/04/04 00:00 [received]
PHST- 2016/06/02 00:00 [accepted]
PHST- 2016/09/08 06:00 [entrez]
PHST- 2016/09/08 06:00 [pubmed]
PHST- 2016/09/08 06:01 [medline]
PHST- 2016/07/21 00:00 [pmc-release]
AID - OL-0-0-4899 [pii]
AID - 10.3892/ol.2016.4899 [doi]
PST - ppublish
SO  - Oncol Lett. 2016 Sep;12(3):2217-2221. doi: 10.3892/ol.2016.4899. Epub 2016 Jul 
      21.