Abstract
Retinoids are known to inhibit the growth of hormone-dependent but not that of hormone-independent breast cancer cells.
We investigated the involvement of retinoic acid (RA) receptors (RARs) in the differential growth-inhibitory effects of retinoids and the underlying mechanism.
Our data demonstrate that induction of RAR beta by RA correlates with the growth-inhibitory effect of retinoids.
The hormone-independent cells acquired RA sensitivity when the RAR beta expression vector was introduced and expressed in the cells.
In addition, RA sensitivity of hormone-dependent cells was inhibited by a RAR beta-selective antagonist and the expression of RAR beta antisense RNA.
Introduction of RAR alpha also restored RA sensitivity in hormone-independent cells, but this restoration was accomplished by the induction of endogenous RAR beta expression.
Furthermore, we show that induction of apoptosis contributes to the growth-inhibitory effect of RAR beta.
Thus, RAR beta can mediate retinoid action in breast cancer cells by promoting apoptosis.
Loss of RAR beta, therefore, may contribute to the tumorigenicity of human mammary epithelial cells.
See also:
- All-Trans-Retinoic Acid (ATRA - analogues and/or derivatives);
- Solution of retinoids in vitamin E in the Di Bella Method biological multitherapy;
- Complete objective response to biological therapy of plurifocal breast carcinoma;
- Pleural Mesothelioma: clinical records on 11 patients treated with Di Bella's Method;
- Malignant pleural mesothelioma, stage T3-T4. Consideration of a case study;