Influence of estrogen, antiestrogen and UV-light on the balance between proliferation and apoptosis in MCP-7 breast adenocarcinoma cells culture

Studies of the mechanism of actions of estrogen, antiestrogen and physical factors may provide clues to an understanding of breast cancer growth and/o r regression regulation and thus identify novel targets for therapeutic int ervention. Defective control of apoptosis appears to play a central role in the pathogenesis of neoplasia. Conversely, cancer therapy and ionizing rad iation can induce cancer cell death by apoptosis and/or necrosis. bcl-2 gen e and p-53 gene products have been both linked to programmed cell death pat hways. We have analyzed the effect of estradiol, tamoxifen and UV exposure on the induction of apoptosis, expression of p53 and bcl-2 gene products as well as the proliferative activity (expressed as [H-3]thymidine incorporat ion and PCNA and MPM2 antigens involvement) in MCF7. It has been found that estradiol increases the speed of cell cycle in MCF7 and acts as antiapoptotic factor. Tamoxifen has multiple influence on the r ate of growth of cancer cells: depends on estrogen receptor (ER), conducts reduction of proliferation rate; depends on ER and other mechanisms conduct s to suppressions of Bcl-2 protein expression and induction of cell death t hrough apoptotic pathway. Estradiol prevents the apoptotic influence of tam oxifen probably by enhancement of Bcl-2 protein expression and does not pre vent the inhibition of proliferation rate. The irradiation with UV induces apoptosis by over-expression of p53 and down-regulation of bcl-2 gene.