Research Papers:

This article has been corrected. Correction in: Oncotarget. 2019; 10:1010.

CLCA4 inhibits bladder cancer cell proliferation, migration, and invasion by suppressing the PI3K/AKT pathway

Teng Hou, Lijie Zhou, Longwang Wang, Gallina Kazobinka, Xiaoping Zhang and Zhaohui Chen _

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Oncotarget. 2017; 8:93001-93013. https://doi.org/10.18632/oncotarget.21724

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Teng Hou1,*, Lijie Zhou1,*, Longwang Wang1,2, Gallina Kazobinka1, Xiaoping Zhang1 and Zhaohui Chen1

1Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

2Department of Urology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, China

*These authors have contributed equally to this work

Correspondence to:

Zhaohui Chen, email: [email protected]

Keywords: CLCA4, bladder cancer, PI3K/Akt, proliferation, metastasis

Received: July 21, 2017    Accepted: August 17, 2017    Published: October 09, 2017


Calcium activated chloride channel A4 (CLCA4), a tumor suppressor, was shown to contribute to the progression of several human cancers, while its role in bladder carcinoma remains unclear. In this study, we showed CLCA4 expression was down-regulated in bladder carcinoma tissues and cells compared to adjacent non-tumor tissues and normal urothelial cells. Low CLCA4 expression was correlated with larger tumor size, advanced tumor stage, and poor prognosis in bladder carcinoma patients. Overexpression of CLCA4 profoundly attenuated the proliferation, growth, migratory and invasive capabilities of bladder cancer cells, whereas CLCA4 knockdown had the opposite effect. Mechanistically, CLCA4 is involved in PI3K/AKT signaling and its downstream molecules can promote bladder cancer cell proliferation. Additionally, CLCA4 could mediate the migration and invasion of bladder cancer cells by regulating epithelial-mesenchymal transition and PI3K/Akt activation. This study suggests that CLCA4 may represent a promising prognostic biomarker for bladder cancer and provides a possible mechanism for bladder cancer growth and invasion.

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