Bcl-2 expression in breast carcinoma cells in vitro

Abstract

Author(s): Jolanta Rzymowska

Apoptosis is a physiological form of cell death that occurs in all tissues Deregulated expression of some oncogenes causes increased cell division and advances cell growth. The balance between bcl-2 and c-myc and c-jun seems to be an important determinant of cellular sensitivity to the induction of apoptosis. Bcl-2 gene promotes cell survival rather than cell proliferation In the our study bcl-2 has been demonstrated to inhibit apoptosis in breast cancer cells in vitro (T47D). High expression of bcl-2 was noticed to be strongly related to low rates of apoptotic and necrotic cell death. The mean value of the apoptotic index was 7.5% in bcl-2-negative tumours and 0.55% in bcl-2-positive tumours. High proliferation rate was associated with the absence of bcl-2 expression. C-myc and c-jun accumulation were associated with the presence of bcl- 2 expression and with decreased apoptotic activity. The loss of bcl-2 expression was strongly correlated with increased apoptotic and necrotic cell death. This establishes a model in which bcl-2 not only mediates in cell death, but also cell division in breast carcinoma cells, and in which the regulation of cell division and cell death are strictly connected.

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