期刊
CANCER LETTERS
卷 253, 期 1, 页码 14-24出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2006.11.019
关键词
retinoids; RAR-beta(2); RAR-beta(4); biomarker; methylation; tumorigenesis
类别
资金
- NCI NIH HHS [R01 CA117895, R29 CA074835-02, R21 CA102265, R01 CA117895-01A2, R29 CA074835, R29 CA74835, R21 CA102265-02, R21 CA10226] Funding Source: Medline
Retinoids, a group of structural and functional analogs of vitamin A, are known to regulate a large number of essential biological processes and to suppress carcinogenesis. The effects of retinoids are mainly mediated by nuclear retinoid receptors, which include retinoic acid receptors (RARs) and retinoid X receptors (RXRs). Each receptor has three subtypes (alpha, beta, and gamma) and each subtype has different isoforms. Retinoic acid receptor-beta (RAR-beta) has four isoforms that have different affinities to retinoids and different biological functions. Loss of expression of RAR-beta(2) during cancer development is associated with tumorigenesis and retinoid resistance; induction of its expression, on the other hand, can suppress carcinogenesis. Expression of another isoform, RAR-beta(4), is increased in various types of cancer. RAR-beta(4) transgenic mice develop hyperplasia and neoplasia in various tissues, and induction of RAR-beta(4) expression increases the growth of tumor cells that do not express RAR-beta(2). Future studies will focus on molecular pathways involving RAR-beta(2) and the role of RAR-beta(4) in cancer development. (C) 2006 Elsevier Ireland Ltd. All rights reserved.
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