Department of Gynecology, Lanzhou University Second Hospital, Lanzhou, 730030, China.
The Second Clinical Medical College of Lanzhou University, Lanzhou, 730000, China.
BMC Mol Cell Biol. 2022 Oct 25;23(1):44. doi: 10.1186/s12860-022-00440-7.
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.
宫颈癌是一种严重威胁全球女性身心健康的恶性肿瘤。钙激活氯离子通道蛋白（CLCA2）作为一种新型钙激活氯离子通道蛋白，在肿瘤的发生发展中发挥着重要作用。但其在宫颈癌中的作用及其确切的调控机制尚不清楚。在本研究中，我们发现 CLCA2 在宫颈癌细胞中明显下调，过表达 CLCA2 抑制宫颈癌细胞的增殖、迁移和侵袭，促进细胞凋亡，CLCA2 通过 p38/JNK/ERK 通路抑制 EMT（上皮间质转化）。体外结果与体内结果一致。综上所述，过表达 CLCA2 抑制了宫颈癌在体内和体外的进展。这可能为 CLCA2 作为宫颈癌临床诊断和预后的新指标或作为药物治疗的潜在靶点提供理论依据。
