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Original Article
- The Role of bcl-2 and p53 in Tamoxifen-Induced Apoptosis of Human Breast Cancer Cell Lines
- Woo Chul Noh, Dong Young Noh, Yong Ho Ham, Chang Min Kim, Nam Sun Paik, Nan Mo Moon, Kuk Jin Choe
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Journal of the Korean Cancer Association 2000;32(3): 531-538.
1Departments of Surgery, Korea Cancer Center Hospital.
2Departments of Laboratory of Molecular Oncology, Korea Cancer Center Hospital.
3Department of Surgery, Seoul National University College of Medicine, Seoul, Korea.
2Departments of Laboratory of Molecular Oncology, Korea Cancer Center Hospital.
3Department of Surgery, Seoul National University College of Medicine, Seoul, Korea.
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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.
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