PMID- 24105047
OWN - NLM
STAT- MEDLINE
DCOM- 20150109
LR  - 20211021
IS  - 1699-3055 (Electronic)
IS  - 1699-048X (Linking)
VI  - 16
IP  - 6
DP  - 2014 Jun
TI  - Peroxiredoxin 3 is resistant to oxidation-induced apoptosis of Hep-3b cells.
PG  - 561-6
LID - 10.1007/s12094-013-1117-y [doi]
AB  - OBJECTIVE: Although peroxiredoxin 3 (PRX3) was reported to be overexpressed in 
      liver cancer, the precise function of PRX3 in the development and/or progression 
      of liver cancer remained to be obscure. The present study was conducted to 
      investigate the response of PRX3 to oxidative stress in hepatocellular carcinoma 
      (HCC) cells. METHODS: After successful knockdown of PRX3 expression by small 
      interfering RNA, we treated HCC cell lines Hep-3b and Hep-G2 with gradient 
      concentrations of H2O2 and detected cell proliferation, apoptosis, and the level 
      of reactive oxygen species (ROS) in the cells. RESULTS: After low-dose (5-20 
      mumol/l) H2O2 treatment, the ROS level was significantly higher in PRX3-knockdown 
      Hep-3b cells than in controls. In addition, PRX3 down-regulation resulted in 
      decreased proliferation, increased apoptosis, and increased caspase 3 activity of 
      Hep-3b cells. We did not notice significant difference between PrxIII knockdown 
      and control Hep-G2 cells in ROS level, cell viability or apoptosis. CONCLUSION: 
      Our results suggest that PRX3 is an indispensable ROS scavenger that protects 
      tumor cells against oxidative damage and subsequent apoptosis, which provides a 
      clue that PRX3 may be involved in the chemotherapeutic resistance of liver 
      cancer. The underlying mechanism for PRX3 function needs further investigation.
FAU - Wang, Y-G
AU  - Wang YG
AD  - Department of Gastroenterology, Shandong Qianfoshan Hospital, Shandong 
      University, Jinan, 250014, China.
FAU - Li, L
AU  - Li L
FAU - Liu, C-H
AU  - Liu CH
FAU - Hong, S
AU  - Hong S
FAU - Zhang, M-J
AU  - Zhang MJ
LA  - eng
PT  - Journal Article
DEP - 20131009
PL  - Italy
TA  - Clin Transl Oncol
JT  - Clinical & translational oncology : official publication of the Federation of 
      Spanish Oncology Societies and of the National Cancer Institute of Mexico
JID - 101247119
RN  - 0 (Oxidants)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Reactive Oxygen Species)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 1.11.1.15 (PRDX3 protein, human)
RN  - EC 1.11.1.15 (Peroxiredoxin III)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - Blotting, Western
MH  - Carcinoma, Hepatocellular/metabolism/*pathology
MH  - Caspase 3/metabolism
MH  - Cell Proliferation/*drug effects
MH  - Flow Cytometry
MH  - Humans
MH  - Hydrogen Peroxide/*pharmacology
MH  - Liver Neoplasms/metabolism/*pathology
MH  - Oxidants/pharmacology
MH  - Oxidation-Reduction
MH  - Peroxiredoxin III/antagonists & inhibitors/genetics/*metabolism
MH  - RNA, Small Interfering/genetics
MH  - Reactive Oxygen Species/*metabolism
MH  - Tumor Cells, Cultured
EDAT- 2013/10/10 06:00
MHDA- 2015/01/13 06:00
CRDT- 2013/10/10 06:00
PHST- 2013/07/02 00:00 [received]
PHST- 2013/09/22 00:00 [accepted]
PHST- 2013/10/10 06:00 [entrez]
PHST- 2013/10/10 06:00 [pubmed]
PHST- 2015/01/13 06:00 [medline]
AID - 10.1007/s12094-013-1117-y [doi]
PST - ppublish
SO  - Clin Transl Oncol. 2014 Jun;16(6):561-6. doi: 10.1007/s12094-013-1117-y. Epub 
      2013 Oct 9.