CLCA2 overexpression suppresses epithelial-to-mesenchymal transition in cervical cancer cells through inactivation of ERK/JNK/p38-MAPK signaling pathways.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS

ACS Applied Bio Materials Pub Date : 2022-10-25 DOI:10.1186/s12860-022-00440-7

Wenhu Xin, Jian Zhang, Haibin Zhang, Xueyao Ma, Yunzhong Zhang, Yufeng Li, Fang Wang

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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.

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CLCA2过表达通过使ERK/JNK/p38-MAPK信号通路失活，抑制宫颈癌细胞上皮向间质转化。

宫颈癌是世界范围内威胁妇女身心健康的重要恶性肿瘤。钙活化氯离子通道(CLCA2)作为一种新型的钙活化氯离子通道蛋白，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和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，CLCA2通过p38 / JNK / ERK通路抑制EMT(上皮-间质转化)。体内实验结果与体外实验结果一致。综上所述，在体内和体外，CLCA2的过表达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药物治疗的潜在靶点提供理论依据。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464