Regulation of Retinoid Responsiveness in Mammary Carcinoma Cells
Final rept. 1 Sep 94-31 Aug 97
COLUMBIA UNIV NEW YORK
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The data presented support our hypothesis that retinoids inhibit human breast cancer cell proliferation by inducing a state of functional mitogen deprivation. Kinetic and quantitative changes in cell cycle progression and gene expression following retinoic acid treatment of the estrogen dependent, T-47D breast cancer cell line, are consistent with retinoic acid inducing a block in the treated cells ability to respond to external mitogenic signals, specifically to epidermal growth factor. The data further implicate protein kinase C alpha as a retinoid induced gene product necessary for inhibiting EGF signaling. By manipulating the expression of the cellular retinoic acid binding protein, type II the cellular retinol binding protein and the nuclear retinoic acid receptor alpha, we also have shown that expression of these mediators of vitamin A action is sufficient to exert growth inhibitory effects on human breast cancer cells in culture.
- Anatomy and Physiology
- Medicine and Medical Research