OVA12 promotes tumor growth by regulating p53 expression in human cancer cells
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Renfeng Zhang1, Xicai Wu2, Xiangfeng Xia3, Asma Khanniche4, Feifei Song5, Bingchang Zhang1, Ying Wang4 and Hailiang Ge4
1Department of Laboratory Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China
2Clinical Laboratory, People’s Hospital of Rizhao, Rizhao, China
3Department of Radiology, The Third People’s Hospital of Rizhao, Rizhao, China
4Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China
5Department of Pathology, Tenth People’s Hospital of Tongji University, Shanghai, China
Bingchang Zhang, email: firstname.lastname@example.org
Ying Wang, email: email@example.com
Hailiang Ge, email: Hailiangsjtu@163.com
Keywords: OVA12, tumor growth, p53
Received: August 04, 2016 Accepted: April 10, 2017 Published: April 28, 2017
Ovarian cancer-associated antigen 12 (OVA12) was first identified in an ovarian carcinoma complementary DNA (cDNA) expression library and has been shown to play an important role in tumor growth. Here, we found that overexpression of OVA12 accelerated tumor growth in different tumor cells, whereas OVA12 depletion was associated with the opposite effect. Moreover, knocking down OVA12 led to a significant increase in the protein levels of p53, and the overexpression of OVA12 significantly decreased endogenous p53 levels. In addition, OVA12 stimulated p53 polyubiquitination and degradation by the proteasome and promoted tumor growth at least partially through the p53 pathway. Taken together, these results indicate that OVA12 is a negative regulator of p53 and that inhibition of OVA12 expression might serve as a therapeutic target to restore tumor suppression.
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