Role of Bcl-2 in Breast Cancer Progression.
Abstract
The anti-apoptotic gene bcl-2 is frequently overexpressed in many human tumors including invasive breast cancer. Involvement of bcl-2 in cancer development was believed to result from its ability to prevent cell death (thereby increasing cell number). We previously showed that bcl-2 deregulates G1/S checkpoint in MCF10A cells, which involves induction of cyclin D1 associated kinase activity. Increasing evidence suggests that overexpression of cyclin D1 contributes to the oncogenic transformation of cells in vitro and in vivo. In the present study, we examined the effects of bcl-2 overexpression on cyclin D1 expression in human breast epithelial cells. Bcl-2 overexpression in MCF10A cells significantly induced expression of cyclin D1 during the cell cycle as determined by an immunoblot analysis. We also show that bcl-2 induction of cyclin D1 expression occurs at the transcriptional level as determined by an assay of cyclin D1 promoter activity. Cyclin D1 reporter activity was induced in a bcl-2 dependent manner in human breast carcinoma cell lines, MCF7 and BT549 as well as in MCF10A. Our previous and present studies suggest that bcl-2 may serve as an oncogene in the development of human breast cancer, which involves induction of cyclin D1 expression.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1998
- Accession Number
- ADA356932
Entities
People
- Hyeong-reh Kim
Organizations
- Wayne State University