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Inhibition of cancer cell growth by all‐ trans retinoic acid and its analog N‐(4‐hydroxyphenyl) retinamide: a possible mechanism of action via regulation of retinoid receptors expression
Author(s) -
Liu Guizhong,
Wu Min,
Levi Giovanni,
Ferrari Nicoletta
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19981005)78:2<248::aid-ijc20>3.0.co;2-5
Subject(s) - retinoid , retinoic acid , biology , cell growth , cancer research , receptor , growth inhibition , endocrinology , apoptosis , retinoic acid receptor , cell culture , medicine , cell , biochemistry , genetics
In order to better understand the mechanisms that underlie the antiproliferative effect of retinoids, we have examined the response of human carcinoma cell lines to all‐ trans retinoic acid (RA) and N‐(4‐hydroxyphenyl) retinamide (4HPR) in terms of cell growth, apoptosis and regulation of retinoic acid receptors (RARs) and retinoid X receptors (RXRs) mRNA. GLC82 (lung adenocarcinoma), BGC823 (stomach adenocarcinoma) and EC109 (esophageal squamous carcinoma) cells were treated with 10 μM of RA or 4HPR for various length of time and analyzed. The results show that growth inhibition by RA and 4HPR in GLC82 and BGC823 cells correlates with the induction of RARβ2 gene, whereas RA resistance in EC109 cells parallels loss of RARβ2 induction. Exogenous RARβ2 expression did not restore RA responsiveness in EC109 cells, but potentiated 4HPR‐induced growth inhibition, suggesting that 4HPR acts at least in part via the RARβ receptor. We speculate that the loss of RARβ2 inducibility in EC109 cells may be due to an unknown repressor. Int. J. Cancer 78:248–254, 1998.© 1998 Wiley‐Liss, Inc.