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ARHGAP24 inhibits cell cycle progression, induces apoptosis and suppresses invasion in renal cell carcinoma

Gaosi Xu _, Xiongbing Lu, Tianlun Huang and Jie Fan

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Oncotarget. 2016; 7:51829-51839. https://doi.org/10.18632/oncotarget.10386

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Abstract

Gaosi Xu1,*, Xiongbing Lu2,*, Tianlun Huang1, Jie Fan1

1Department of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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

*These authors have contributed equally to this work

Correspondence to:

Gaosi Xu, email: [email protected]

Keywords: renal cancer, ARHGAP24, proliferation, cell cycle, apoptosis

Received: March 14, 2016     Accepted: June 13, 2016     Published: July 2, 2016

ABSTRACT

Renal cell carcinoma (RCC) is the major cause of kidney malignancy-related deaths. Rho GTPases are key regulators in cancer cell metastasis. ARHGAP24, a Rac-specific member of the Rho GTPase-activating protein family, acts as a functional target of cancer cell migration and invasion. In the present study, we identified ARHGAP24 expression is downregulated in renal cancer tissues and is highly correlated with long-term survival in RCC patients. Therefore, we investigated the biological functions of ARHGAP24 in renal cancer cells. Ectopic expression of ARHGAP24 resulted in inhibited cell proliferation and arrested cell cycle in two renal cancer cell lines (786-0 and Caki-2); the results were confirmed by ARHGAP24 knocking down. In addition, ARHGAP24 significantly reduced the cell invasion ability and induced apoptosis in renal cancer cells. In addition, overexpressing ARHGAP24 impaired tumor formation in vivo. In summary, our results illustrated that ARHGAP24 plays a unique role in RCC progression as a tumor repressor.


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