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• W1567508417 abstract "Abstract : Retinoids, the natural and synthetic vitamin A derivatives, are promising chemopreventive agents against breast cancer. However, the molecular mechanisms by which trans-retinoic acid (RA) exerts its anticancer effects and how the effects are lost in certain estrogen-independent breast cancer cells are largely unknown. Our data demonstrate that RA receptor (RAR) B plays a critical role in mediating the growth inhibitory effect of trans-RA, whereas the anti-cancer effect of RARa may be due to its induction of RAR alpha. In addition, we found that retinoid X receptor (RXR)-selective retinoids could inhibit the growth of estrogen-independent, RARcx-negative, trans-RA-resistant breast cancer cells. The effects of RXR-selective retinoids are likely mediated by RXRInur77 heterodimers that bind to and activate RAR% promoter. RXRInur77 heterodimers are preferentially formed in the absence of RAR alpha, suggesting that levels of RARa determine the formation of RXR/rar or RXRInur77 heterodimers and switch of retinoid growth inhibition pathways. Together, our results reveal a novel retinoid growth inhibition pathway through activation of RXR and provide a new approach to inhibit the growth of estrogen-independent breast cancer cells. Our data also demonstrate that RAR beta can be activated by different retinoid receptor dimeric complexes and act to mediate the growth inhibitory effects of various retinoids." @default.
• W1567508417 created "2016-06-24" @default.
• W1567508417 creator A5049585151 @default.
• W1567508417 date "1995-10-01" @default.
• W1567508417 modified "2023-09-26" @default.
• W1567508417 title "Mechanism of Retinoid Response in Human Breast Cancer." @default.
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• W1567508417 doi "https://doi.org/10.21236/ada303373" @default.
• W1567508417 hasPublicationYear "1995" @default.
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