Abstract：
Cervical cancer is an important malignant tumor threatening the physical and mental health of women in the world. As a new calcium activated chloride channel protein, calcium activated chloride channel (CLCA2) plays an important role in tumorigenesis and development. But its role and exact regulatory mechanism in cervical cancer are still unclear. In our study, we found CLCA2 was significantly decreased in cervical cancer cells, and overexpression of CLCA2 inhibited the proliferation, migration and invasion, and promotes apoptosis of cervical cancer cells, and CLCA2 inhibited EMT (Epithelial-mesenchymal transition) through an p38 / JNK / ERK pathway. The results in vivo were consistent with those in vitro. In conclusion, overexpression of CLCA2 inhibited the progression of cervical cancer in vivo and in vitro. This may provide a theoretical basis for CLCA2 as a new indicator of clinical diagnosis and prognosis of cervical cancer or as a potential target of drug therapy.
摘要：
宫颈癌是全球范围内威胁女性身心健康的重要恶性肿瘤。作为一种新的钙激活氯离子通道蛋白，钙激活氯通道(CLCA2)在肿瘤发生、发展中起着重要作用。但其在宫颈癌中的作用及确切调控机制尚不清楚。在我们的研究中,我们发现CLCA2在宫颈癌细胞中显著降低,CLCA2的过表达抑制细胞增殖，移民和入侵，促进宫颈癌细胞凋亡，CLCA2通过p38/JNK/ERK途径抑制EMT（上皮-间质转化）。体内结果与体外结果一致。总之,CLCA2的过表达在体内和体外抑制了宫颈癌的进展。这可能为CLCA2作为宫颈癌临床诊断和预后的新指标或作为潜在的药物治疗靶点提供理论依据。
