Knockdown of mutated ARID1A inhibited endometrial cancer cell proliferation and stimulated cell apoptosis
Ye, Y.; Wei, B.; Xiaowei, X.
Journal of BUON Official Journal of the Balkan Union of Oncology 23(4): 1082-1091
2018
ISSN/ISBN: 1107-0625 PMID: 30358215 Document Number: 697356
Mutations in the gene encoding the AT-rich interacting domain containing protein 1A (ARID1A) are frequently observed in endometrial cancer, although the molecular mechanisms linking the genetic changes remain poorly understood. This study aimed to elucidate the influence of ARID1A mutations on endometrial cancer cells and tissues. Reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blot and immunohistochemistry (IHC) were used to investigate the expression of ARID1A in endometrial cancer cells and tissues. Lentiviral vector (LV)-shARID1A was constructed and transfected into HEC-1-A cells. The efficiency of mutated ARID1A knockdown was determined by RT-qPCR and western blotting. The proliferation and apoptosis capacity was examined by colony formation, MTT proliferation, Annexin V-APC cell apoptosis and cell cycle analysis. ARID1A was lower in endometrial cancer cells and endometrial carcinoma tissue than in normal endometrial cells and benign endometrium (p<0.05). Small interfering RNA (siRNA)-ARID1A were transfected into HEC-1-A cells and we observed reduced cell growth and proliferation, increased apoptosis, and a significantly increased proportion of cells in the G2/M phase. Our results suggest that ARID1A mutation in endometrial cancer helped cell proliferation and inhibited cell apoptosis and also caused cell cycle arrest at the G2/M phase.