The Role of bcl-2 and p53 in Tamoxifen-Induced Apoptosis of Human Breast Cancer Cell Lines.
- Author:
Woo Chul NOH
1
;
Dong Young NOH
;
Yong Ho HAM
;
Chang Min KIM
;
Nam Sun PAIK
;
Nan Mo MOON
;
Kuk Jin CHOE
Author Information
1. Departments of Surgery, Korea Cancer Center Hospital.
- Publication Type:Original Article
- Keywords:
Apoptosis;
bcl-2 protein;
Breast neoplasm;
p53 protein;
Tamoxifen
- MeSH:
Apoptosis*;
Breast Neoplasms*;
Breast*;
Cell Line*;
Down-Regulation;
Humans*;
MCF-7 Cells;
Phenotype;
Prognosis;
Tamoxifen
- From:Journal of the Korean Cancer Association
2000;32(3):531-538
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Tamoxifen has been well known as an effective anti-tumor agent against breast cancer. The important role of bcl-2 and p53 proteins in tamoxifen-induced apoptosis of breast cancer cells has been suggested. However, the paradoxical fact that bcl-2 over-expression is assdegrees Ciated with better prognosis in clinic has not yet been clearly explained. To investigate this paradox, we analyzed the effect and dynamics of bcl-2 and p53 on the apoptosis after treatment of breast cancer cells with tamoxifen. MATERIALS AND METHODS: The human breast cancer cell lines MCF-7 and MB MDA-468 were treated with 17-betaestradiol (E2) and tamoxifen. RESULTS: Following tamoxifen treatment, MCF-7 cells underwent apoptosis accompanied by reduced bcl-2 expression. E2 pre-treatment led to the inhibition of tamoxifen-mediated apoptosis and bcl-2 down-regulation. When MB MDA-468 cells were treated with E2 or tamoxifen, bcl-2 and p53 protein expression did not change and apoptosis did not develop. CONCLUSION: We observed that the down-regulation of bcl-2 by tamoxifen treatment can facilitate the apoptosis of breast cancer cells without p53 mutations. This finding was consistent with clinical experiences in which bcl-2 positive tumors were assdegrees Ciated with more indolent phenotypes in breast cancer.
