RESUMO

Gestational trophoblastic diseases, like the complete hydatidiform mole (CHM), are a group of human interrelated neoplasms whose etiology and progression is poorly understood at the molecular level. We have previously reported the cloning and expression of a new tumor necrosis factor receptor (TNF-R) related transcript, named CHMS-1 that encodes a potential death domain. Here we show that ectopic expression of the putative CHMS-1 death domain specifically induced apoptosis in a dose-dependent manner, in trophoblastic (JEG-3) and non-trophoblastic (COS-7) cells. We also investigated the expression of apoptosis-related molecules such as Bcl-2 and p53 and demonstrated that Bcl-2 is repressed in CHM while p53 is overexpressed in CHM compared with persistent gestational trophoblastic tumors. Altogether, these data indicate that the CHMS-1 death domain is able to trigger apoptosis, thus suggesting that this new entity might be an important inducer of molar regression mechanisms in women.

Assuntos

Apoptose , Proteínas de Neoplasias/metabolismo , Receptores do Fator de Necrose Tumoral/metabolismo , Trofoblastos/metabolismo , Animais , Northern Blotting , Feminino , Citometria de Fluxo , Expressão Gênica , Proteínas de Fluorescência Verde , Humanos , Técnicas Imunoenzimáticas , Proteínas Luminescentes/metabolismo , Proteínas de Neoplasias/genética , Gravidez , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , RNA Mensageiro/metabolismo , Receptores do Fator de Necrose Tumoral/genética , Proteínas Recombinantes de Fusão/metabolismo , Transfecção , Trofoblastos/patologia , Células Tumorais Cultivadas/metabolismo , Células Tumorais Cultivadas/patologia , Proteína Supressora de Tumor p53/metabolismo