17 beta -Estradiol induces ER beta up-regulation via p38/MAPK activation in colon cancer cells

• Published in: Biochemical and biophysical research communications Vol. 359; no. 1; pp. 102 - 107
• Main Authors: Caiazza, F, Galluzzo, P, Lorenzetti, S, Marino, M
• Format: Journal Article
• Language: English
• Published: 20.07.2007
• ISSN: 0006-291X
• DOI: 10.1016/j.bbrc.2007.05.059

Estrogen receptors (ER alpha and ER beta ) mediate opposite functions on cancer growth induced by 17 beta -estradiol (E2). E2 binding to ER alpha induces a cancer promoting response, whereas E2 binding to ER beta exerts a protective action against cancer growth. Moreover, E2 can diversely modulate the ER alpha and ER beta levels intensifying or decreasing their actions in target tissues. Only molecular mechanisms at the root of E2 ability to down-regulate the ER alpha levels are known. Here, we report the first molecular mechanism underlying E2-induced ER beta up-regulation in DLD-1 colon cancer cells. E2 induces a short term (2 and 4h after stimulation) translation of ER beta mRNA followed by a late (24h after stimulation) enhanced transcription. Both processes required the E2-induced persistent and palmitoylation-dependent p38/MAPK activation. Overall, our data suggest a finely tuned control exerted by rapid signals on different cellular molecular events important for the protective effects of E2 against colon cancer growth.