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.
|Number of pages||7|
|Journal||International Journal of Cancer|
|Publication status||Published - 1998|
ASJC Scopus subject areas
- Cancer Research