Vitamin A and apoptosis in prostate cancer

Zhang, XK

HERO ID

1490132

Reference Type

Journal Article

Subtype

Review

Year

2002

Language

English

PMID

12121833

HERO ID 1490132
Material Type Review
In Press No
Year 2002
Title Vitamin A and apoptosis in prostate cancer
Authors Zhang, XK
Journal Endocrine-Related Cancer
Volume 9
Issue 2
Page Numbers 87-102
Abstract Apoptosis represents an effective way to eliminate cancer cells. Unfortunately, advanced prostate tumors eventually progress to androgen-independent tumors, which are resistant to current therapeutic approaches that act by triggering apoptosis. Vitamin A and its natural and synthetic analogs (retinoids) induce apoptosis in prostate cancer cells in vitro and in animal models, mainly through induction of retinoic acid receptor-beta (RARbeta). Expression levels of RARbeta, however, are significantly reduced in hormone-independent prostate cancer cells. Recently, a new class of synthetic retinoids related to 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (AHPN) (also called CD437) that effectively induces apoptosis of both hormone-dependent and -independent prostate cancer cells in a retinoid receptor-independent manner was identified and has drawn a lot of attention in the field. The apoptotic effect of AHPN requires expression of orphan receptor TR3 (also called nur77 or NGFI-B). Paradoxically, TR3 expression is also induced by androgen and other mitogenic agents in prostate cancer cells to confer their proliferation. The recent finding that TR3 migrates from the nucleus to mitochondria to trigger apoptosis in response to AHPN suggests that the opposing biological activities of TR3 are regulated by its subcellular localization. Thus, agents that induce translocalization of TR3 from the nucleus to mitochondria will have improved efficacy against prostate cancer. TR3, therefore, represents an unexplored molecule that may be an ideal target for developing new agents for prostate cancer therapy.
Doi 10.1677/erc.0.0090087
Pmid 12121833
Wosid WOS:000177100200002
Url https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036327656&doi=10.1677%2ferc.0.0090087&partnerID=40&md5=57788d252a484947c8042232205e48e4
Is Certified Translation No
Dupe Override No
Comments Source: Web of Science WOS:000177100200002
Is Public Yes
Language Text English