NCOA5通过调控上皮间质转化促进卵巢癌细胞的侵袭转移能力

NCOA5 promotes the invasion and metastasis of ovarian cancer cells by regulating Epithelial-mesenchymal transition

目的研究核受体共激活因子5(NCOA5)对卵巢癌细胞侵袭和转移能力的作用及分子机制。方法常规培养卵巢癌细胞株SKOV-3、A2780、OC3、HO-8910和正常卵巢上皮细胞系IOSE80,Western blot检测各细胞中NCOA5蛋白的表达水平。选取高表达NCOA5的卵巢癌细胞SKOV-3和A2780,各分为si-NC组、si-NCOA5组,并分别转染NC siRNA和NCOA5 siRNA。Boyden实验检测各组细胞侵袭能力,Transwell实验检测各组细胞转移能力,Western blot检测各组细胞上皮间质转(EMT)相关蛋白E-cadherin、N-cadherin、vimentin和Slug蛋白的表达水平。结果Western blot结果显示NCOA5在卵巢癌细胞中的表达显著上调(P<0.05)。在SKOV-3和A2780细胞中干扰NCOA5的表达均显著抑制卵巢癌细胞侵袭和转移能力(P<0.05),并促进EMT相关蛋白E-cadherin的表达,抑制细胞中EMT相关蛋白N-cadherin、vimentin和Slug蛋白的表达(P<0.05)。结论NCOA5促进卵巢癌侵袭转移能力,具有作为卵巢癌新型预后生物标志物和治疗分子靶点的潜力。

Objective To study the role of Nuclear Receptor Coactivator 5(NCOA5)on ovarian cancer cells and molecular mechanisms.Methods Ovarian cancer cell lines SKOV-3,A2780,OC3,HO-8910 and normal ovarian epithelial cell line IOSE80 were cultured regularly.Western blot analysis was performed to detect the expression level of NCOA5 protein in each cell line.Ovarian cancer cells SKOV-3 and A2780 with high expression of NCOA5 were selected and divided into si-NC group and si-NCOA5 group,respectively,and transfected with NC siRNA and NCOA5 siRNA,respectively.Boyden assay was used to detect cell invasion ability,Transwell assay was used to detect cell metastasis ability,and Western blot assay was used to detect the expression levels of EMT-related proteins E-cadherin,N-cadherin,vimentin and Slug.Results Western blot results show that the expression of NCOA5 in ovarian cancer cells were significantly increased(P<0.05).The expression of interference NCOA5 significantly inhibited ovarian cancer cell invasion and metastasis(P<0.05),and promoted the expression of EMT-related protein E-Cadherin,inhibited the expression of EMT-related protein N-Cadherin,Vimentin,and Slug protein in cells(P<0.05).Conclusion NCOA5 promotes the metastasis of ovarian cancer invasion and has the potential to be a new type of prognosis of ovarian cancer and the potential for the treatment of molecular targets.