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; Zhaohui Chen

doi:10.18632/oncotarget.21724

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

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 _

PDF | HTML | Supplementary Files | How to cite | Press Release

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

Metrics: PDF 1575 views | HTML 2866 views | ?

Abstract

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

ABSTRACT

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.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 21724

Publication Alerts

Research Papers:

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

Abstract