We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Survival versus apoptotic 17-estradiol effect: Role of ERa and ER activated non-genomic signaling.
- Authors
Filippo Acconcia; Pierangela Totta; Sumito Ogawa; Irene Cardillo; Satoshi Inoue; Stefano Leone; Anna Trentalance; Masami Muramatsu; Maria Marino
- Abstract
The capability of 17-estradiol (E2) to induce the non-genomic activities of its receptors (ERa and ER) and to evoke different signaling pathways committed to the regulation of cell proliferation has been analyzed in different cell cancer lines containing transfected (HeLa) or endogenous (HepG2, DLD1) ERa or ER. In these cell lines, E2 induced different effects on cell growth/apoptosis in dependence of ER isoforms present. The E2ERa complex rapidly activated multiple signal transduction pathways (i.e., ERK/MAPK, PI3K/AKT) committed to both cell cycle progression and apoptotic cascade prevention. On the other hand, the E2ER complex induced the rapid and persistent phosphorylation of p38/MAPK which, in turn, was involved in caspase-3 activation and cleavage of poly(ADP-ribose)polymerase, driving cells into the apoptotic cycle. In addition, the E2ER complex did not activate any of the E2ERa-activated signal molecules involved in cell growth. Taken together, these results demonstrate the ability of ER isoform to activate specific signal transduction pathways starting from plasma membrane that may justify the effect of E2 in inducing cell proliferation or apoptosis in cancer cells. In particular this hormone promotes cell survival through ERa non-genomic signaling and cell death through ER non-genomic signaling. 2004 Wiley-Liss, Inc.
- Subjects
REGULATION of cell growth; CELL cycle; APOPTOSIS; BACTERIOPHAGES
- Publication
Journal of Cellular Physiology, 2005, Vol 203, Issue 1, p193
- ISSN
0021-9541
- Publication type
Article
- DOI
10.1002/jcp.20219