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GNA14 silencing suppresses the proliferation of endometrial carcinoma cells through inducing apoptosis and G(2)/M cell cycle arrest

Endometrial carcinoma is the most common gynecological malignancy. The pathological factors triggering this disease are largely unknown. Although the role of guanine nucleotide-binding protein subunit α (GNA) 11 (GNA11) in melanoma has been described, the involvement of GNA14 in endometrial carcinom...

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Detalles Bibliográficos
Autores principales: Wang, Jing, Lv, Xiao, Xu, Feixue, Wei, Min, Liu, Cuiping, Yang, Yongxiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6127665/
https://www.ncbi.nlm.nih.gov/pubmed/30054423
http://dx.doi.org/10.1042/BSR20180574
Descripción
Sumario:Endometrial carcinoma is the most common gynecological malignancy. The pathological factors triggering this disease are largely unknown. Although the role of guanine nucleotide-binding protein subunit α (GNA) 11 (GNA11) in melanoma has been described, the involvement of GNA14 in endometrial carcinoma remains to be determined. Here, we found that GNA14 expression was increased in endometrial carcinoma tissues compared with simple hyperplasia tissues. Based on lentivirus-mediated knockdown assay, we showed that GNA14 silencing significantly suppressed the proliferation of both HEC-1-A and Ishikawa cells. The caspase 3/caspase 7 activity and apoptosis were enhanced by GNA14 knockdown. GNA14 depletion led to cell cycle arrest at the G(2)/M phase. In addition, Apoptosis Array analysis revealed that caspase-3 and Fas were up-regulated by GNA14 knockdown. Our study suggests that GNA14 silencing blunts endometrial carcinoma cell proliferation. Targetting GNA14 may bring help for the patients of endometrial carcinoma.