TAILIEUCHUNG - Báo cáo khoa học: Dehydroepiandrosterone inhibits the proliferation and induces the death of HPV-positive and HPV-negative cervical cancer cells through an androgen- and estrogen-receptor independent mechanism

Dehydroepiandrosterone (DHEA) has a protective role against epithelial-derived carcinomas; however, the mechanisms remain unknown. We deter-mined the effect of DHEA on cell proliferation, the cell cycle and cell death in three cell lines derived from human uterine cervical cancers infected or not with human papilloma virus (HPV). | Dehydroepiandrosterone inhibits the proliferation and induces the death of HPV-positive and HPV-negative cervical cancer cells through an androgen- and estrogen-receptor independent mechanism Roma A. Girton1 Luis F. Montano2 Maria L. Escobar3 and Rebeca Lopez-Marure1 1 Departamento de Biologia Celular Institute Nacionalde Cardiologia Ignacio Chavez Mexico . Mexico 2 Laboratorio de Inmunobiologia Departamento de Biologia Celular y Tisular Facultad de Medicina Universidad NacionalAutonoma de Mexico UNAM Mexico 3 Departamento de Biologia Celular Facultad de Ciencias Universidad NacionalAutonoma de Mexico UNAM Mexico Keywords androgen receptor cell proliferation DHEA estrogen-receptor HPV Correspondence R. Lopez-Marure Departamento de Biologia Celular Instituto Nacionalde Cardiologia Ignacio Chavez Juan Badiano No. 1 Colonia Seccion 16 Tlalpan . 14080 Mei xico . Mexico Fax 52 55 73 09 26 Tel 52 55 73 29 11 ext. 1337 E-mail rlmarure@ Received 3 June 2009 revised 21 July 2009 accepted 30 July 2009 doi Dehydroepiandrosterone DHEA has a protective role against epithelial-derived carcinomas however the mechanisms remain unknown. We determined the effect of DHEA on cell proliferation the cell cycle and cell death in three cell lines derived from human uterine cervical cancers infected or not with human papilloma virus HPV . We also determined whether DHEA effects are mediated by estrogen and androgen receptors. Proliferation of C33A HPV-negative CASKI HPV16-positive and HeLa HPV18-positive cells was evaluated by violet crystal staining and 3- 4 5-dimethylthiazol-2-yl -2 5-diphenyl-tetrazolium bromide MTT reduction. Flow cytometry was used to evaluate the phases of the cell cycle and cell death was detected using a commercially available carboxyfluorescein apoptosis detection kit that determines caspase activation. DNA fragmentation was determined using the terminal deoxynucleotidyl transferase dUTP nick-end labeling TUNEL

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