Protective Role of Prx(Peroxiredoxin) I and II against H2O2-Induced Apoptosis of MCF7 Cell Lines.
10.4048/jkbcs.2003.6.2.68
- Author:
Soo Jung AHN
1
;
Ji Yeon BAE
;
Ryung Ah LEE
;
Wonshik HAN
;
Seok Won KIM
;
Ho Zoon CHAE
;
Dong Young NOH
Author Information
1. Department of Surgery, College of Medicine, Seoul National University, Seoul, Korea. dynoh@plaza. snu.ac. kr.
- Publication Type:Original Article
- Keywords:
Prx(peroxiredoxin);
H2O2;
Breast cancer;
Apoptosis;
Oxidative stress
- MeSH:
Antibodies;
Apoptosis*;
Breast;
Breast Neoplasms;
Cell Death;
Cell Line;
Clinical Coding;
Free Radicals;
Hydrogen Peroxide;
MCF-7 Cells*;
Metabolism;
Oxidative Stress;
Oxygen;
Peroxides;
Peroxiredoxins;
Protein Isoforms;
RNA, Messenger
- From:Journal of Korean Breast Cancer Society
2003;6(2):68-74
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Apoptosis is known to be induced either by direct oxidative damage from oxygen free radicals or hydrogen peroxide, or from their generation in cells by injurious agents. Peroxiredoxin plays an important role in eliminating peroxides generated during metabolism. The aim of this study is to elucidate the role of Prx (peroxiredoxin) enzymes during the cellular response to oxidative stress. METHODS: The presence of Prx isoforms was demonstrated by immunoblot analysis using Prx isoforms-specific antibodies, and RT-PCR using Prx isozyme coding sequences. Annexin V-FITO apoptosis detection method was used to measure the cell death following exposure to H2O2. RESULTS: Treatment of MCF7 cell lines with H2O2 resulted in the dose-dependent expression of Prx I and II. Observed decreases in the mRNA expressions of Prx I and II, analyzed by RT-PCR, correlated well with the results of immunoblot analysis. The treatment of normal breast cell line, MCF10A, with H2O2 resulted in rapid cell death, while the breast cancer cell line, MCF7, was resistant. In addition, we confirmed that Prx I and II transfected MCF10A cells were more prone to cell death than MCF10A transfected with vector alone, after H2O2 treatment. CONCLUSION: These findings suggest that Prx I and II have an important function as inhibitors of cell death during the cellular response to oxidative stress.
