TBX2基因沉默抑制卵巢癌细胞增殖同时促进细胞衰老发生

TBX2 Gene Silencing Inhibits Cell Proliferation and Promotes Cellular Senescence in Ovarian Cancer Cells

卵巢癌已成为致死率最高的妇科恶性肿瘤,缺乏特异性分子靶点是引起其高致死率的重要因素之一.TBX2是发育相关转录因子T-box基因家族成员之一,已证实其在黑色素瘤等多种肿瘤中异常表达.本实验通过免疫组化检测了人良性卵巢囊肿组织与卵巢癌组织中TBX2蛋白表达,并采用CCK8法、克隆形成实验、SA-β-Gal染色等方法,分析了在卵巢癌细胞中敲低TBX2后对细胞增殖和衰老的影响.结果表明TBX2在卵巢癌组织中高表达,同时TBX2基因沉默抑制了卵巢癌细胞增殖和克隆形成,诱导了P21WAF1和P16INK4A表达上调,促进了细胞衰老发生.

Ovarian cancer is the most lethal malignant gynecological tumor and the absence of specific molecular targets is one of the key factors. TBX2 belongs to the developmentally related T-box family of transcription factors and has been confirmed abnormal expression in several cancers such as melanoma. Inthis study, we detected TBX2 protein expression between benign tumor tissues and malignant ovarian cancer tissues by IHC. Then, We constructed TBX2 stably knocked down ovarian cancer cell lines by RNAi technique. Subsequently, cell proliferation were analyzed by CCK8 assay and colony forming ability in TBX2 gene silencing cells. cellular senescence were detected by SA-β-galactosidase staining and the differential expression of typical senescence-associated genes such as P21^（WAF1） and P16^（INK4A）.The results showed that TBX2 is highly expressed in malignant ovarian cancer tissues. Furthermore, TBX2 silencing inhibits cell proliferation and colony formation, induces the up-regulation of P21^（WAF1） and P16^（INK4A） expression and promotes cellular senescence.