Retinoid, retinoic acid receptor beta and breast cancer.

Abstract

Retinoids have been reported to inhibit the growth of several breast cancer cell lines in culture and to reduce breast tumor growth in animal models. Furthermore, retinoic acid (RA) can augment the action of other breast cancer cell growth inhibitors both in vitro and in vivo. Clinically, interest has increased in the potential use of retinoids for the prevention and treatment of human breast cancer. The regulation of cell growth and differentiation of normal, premalignant, and malignant cells by retinoids is mediated by the RA receptors (RARs) and retinoid X receptor. One of the target genes of retinoid receptors is RARbeta2. A growing body of evidence supports the hypotheses that the RARbeta2 gene is a tumor suppressor gene and the chemopreventive effects of retinoids are due to induction of RARbeta2. RARbeta2 expression is reduced in many malignant tumors including breast carcinoma. This paper will briefly discuss basic aspects of retinoids and retinoid acid receptor. In particular, we review what is now known for inactivation mechanism of RARbeta2 and its role in tumor cell growth inhibition.

• Authors: Qifeng Yang, Takeo Sakurai, Kennichi Kakudo
• Journal: Breast cancer research and treatment (Breast Cancer Res Treat) Vol. 76 Issue 2 Pg. 167-73 (Nov 2002) ISSN: 0167-6806 [Print] Netherlands
• PMID: 12452454 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Receptors, Retinoic Acid
• Retinoids
• retinoic acid receptor beta
• Tretinoin

Topics

• Breast Neoplasms (drug therapy, metabolism, prevention & control)
• Gene Expression Regulation, Neoplastic (drug effects)
• Genes, Tumor Suppressor
• Humans
• Receptors, Retinoic Acid (genetics, metabolism)
• Retinoids (therapeutic use)
• Tretinoin (therapeutic use)
• Tumor Cells, Cultured
• Up-Regulation