CLCA2 overexpression suppresses epithelial-to-mesenchymal transition in cervical cancer cells through inactivation of ERK/JNK/p38-MAPK signaling pathways.
CLCA2 overexpression suppresses epithelial-to-mesenchymal transition in cervical cancer cells through inactivation of ERK/JNK/p38-MAPK signaling pathways.
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CLCA2过表达通过灭活ERK/JNK/p38-MAPK信号通路来抑制宫颈癌细胞中的上皮 - 间质转变。
DOI：
10.1186/s12860-022-00440-7
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发表时间：
2022-10-25
影响因子：
2.8
通讯作者：
中科院分区：
文献类型：
--
作者：
宫颈癌是世界范围内威胁妇女身心健康的重要恶性肿瘤。钙激活氯离子通道（CLCA 2）作为一种新的钙激活氯离子通道蛋白，在肿瘤的发生发展中起着重要作用。但其在宫颈癌中的作用及确切的调控机制尚不清楚。我们的研究发现CLCA 2在宫颈癌细胞中表达显著降低，CLCA 2过表达抑制宫颈癌细胞的增殖、迁移和侵袭，促进宫颈癌细胞凋亡，CLCA 2通过p38 / JNK / ERK通路抑制EMT（Epithelial-mesenchymal transition）。体内实验结果与体外实验结果一致。总之，CLCA 2的过表达在体内和体外抑制宫颈癌的进展。这可能为CLCA 2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。
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.
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