INVESTIGADORES
MERESMAN Gabriela Fabiana
congresos y reuniones científicas
Título:
Protein expression and cellular localization of estrogen receptors alpha and beta in endometriosis-associated epithelial ovarian cancer cell lines.
Autor/es:
BASTON JI; FERELLA L; SINGLA JJ; GONZALEZ A; MERESMAN G
Lugar:
Ciudad Autónoma de Buenos Aires
Reunión:
Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017
Resumen:
The potential role of the estradiol secreted by endometriotic lesions on the pathophysiological mechanisms of endometriosis-associated epithelial ovarian cancer (E-AEOC), such as endometrioid and clear-cell epithelial ovarian tumors, is not yet entirely known. So, the main objective of this study was to evaluate the protein expression and cellular localization of Estrogen Receptors alpha (ERα) and beta (ERβ) in cell lines derived from human E-Aendomteriosis-associated EOCs. Human TOV-112D cell line derived from an endometrioid-type ovarian carcinoma and human TOV-21G cell line derived from a clear-cell ovarian carcinoma were cultured under standard conditions until confluence to further analysis of ERα and ERβ protein expression and cellular localization, in 4 independent experiments, by Western blot and indirect immunofluorescence (IFI) respectively. We found that both endometriosis-associated ovarian cell lines expressed the canonical steroid receptor proteins, being the ERα expression stronger than ERβ in both cell lines. In addition, the ERα was mainly localized into the cellular nucleus, whereas ERβ was mostly localized into cytoplasm. These results suggest that these cell lines are endowed with the necessary molecular machinery to respond to estradiol, becoming them as a suitable in vitro model to study the potential role of steroid hormones secreted by endometriotic lesions on the onset and development of endometriosis-associated EOC. This is an initial descriptive study, so functional studies will be addressed to fully understand the role of the estradiol secreted by endometriotic lesion on the pathophysiological mechanisms underlying the etiology of endometriosis-associated EOC