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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hadadi, Agreen Chaudhri, Reyhaan A. Boyan, Barbara D. Lobachev, Kirill S. Schwartz, Zvi |
| Description | Author Affiliation: Chaudhri RA ( The School of Biology and the Petit Institute for Bioengineering and Biosciences, Georgia Institute of Technology, Atlanta, GA, USA); Hadadi A ( The School of Biology and the Petit Institute for Bioengineering and Biosciences, Georgia Institute of Technology, Atlanta, GA, USA.); Lobachev KS ( The School of Biology and the Petit Institute for Bioengineering and Biosciences, Georgia Institute of Technology, Atlanta, GA, USA.); Schwartz Z ( School of Engineering, Virginia Commonwealth University, Richmond, VA, USA.); Boyan BD ( The School of Biology and the Petit Institute for Bioengineering and Biosciences, Georgia Institute of Technology, Atlanta, GA, USA) |
| Abstract | 17ß-Estradiol can promote the growth and development of several estrogen receptor (ER)-negative breast cancers. The effects are rapid and non-genomic, suggesting that a membrane-associated ER is involved. ER 36 has been shown to mediate rapid, non-genomic, membrane-associated effects of 17ß-estradiol in several cancer cell lines, including triple negative HCC38 breast cancer cells. Moreover, the effect is anti-apoptotic. The aim of this study was to determine if ER 36 mediates this anti-apoptotic effect, and to elucidate the mechanism involved. Taxol was used to induce apoptosis in HCC38 cells, and the effect of 17ß-estradiol pre-treatment was determined. Antibodies to ER 36, signal pathway inhibitors, ER 36 deletion mutants, and ER 36-silencing were used prior to these treatments to determine the role of ER 36 in these effects and to determine which signaling molecules were involved. We found that the anti-apoptotic effect of 17ß-estradiol in HCC38 breast cancer cells is in fact mediated by membrane-associated ER 36. We also showed that this signaling occurs through a pathway that requires PLD, LPA, and PI3K; G s and calcium signaling may also be involved. In addition, dynamic palmitoylation is required for the membrane-associated effect of 17ß-estradiol. Exon 9 of ER 36, a unique exon to ER 36 not found in other identified splice variants of ER with previously unknown function, is necessary for these effects. This study provides a working model for a mechanism by which estradiol promotes anti-apoptosis through membrane-associated ER 36, suggesting that ER 36 may be a potential membrane target for drug design against breast cancer, particularly triple negative breast cancer. |
| ISSN | 00063002 |
| Journal | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |
| Issue Number | 11 |
| Volume Number | 1843 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-11-01 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Biochemistry |
| Content Type | Text |
| Resource Type | Article |
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