GNA14 silencing suppresses the proliferation of endometrial carcinoma cells through inducing apoptosis and G2/M cell cycle arrest

被引:10
作者
Wang, Jing [1 ]
Lv, Xiao [1 ]
Xu, Feixue [1 ]
Wei, Min [1 ]
Liu, Cuiping [1 ]
Yang, Yongxiu [1 ]
机构
[1] Lanzhou Univ, Dept Obstet & Gynecol, Hosp 1, Lanzhou 730000, Gansu, Peoples R China
关键词
K-RAS MUTATIONS; SEROUS CARCINOMA; EXPRESSION; PATHWAY; RASGRP3;
D O I
10.1042/BSR20180574
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 a (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.
引用
收藏
页数:11
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