Research Papers:
C23 promotes tumorigenesis via suppressing p53 activity
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Abstract
Qun Li1,*, Yan Zhu2,*, Lili Hou3,*, Juan Wang4, Guilin Hu5, Xing Fang6, Yamin Hu6, Tingting Tao6, Xin Wei6, Haitao Tang6, Baojun Huang1, Wanglai Hu1
1Department of Immunology, Anhui Medical University, Hefei, China
2Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, China
3Department of Clinical Nutriology, The First Affiliated Hospital of Anhui Medical University, Hefei, China
4Department of Molecular Biology, Shanxi Cancer Hospital and Institute, Affiliated Hospital of Shanxi Medical University, Taiyuan, China
5School of Life Sciences, Anhui Medical University, Hefei, China
6School of Pharmacy, Anhui Medical University, Hefei, China
*These authors have contributed equally to this work
Correspondence to:
Wanglai Hu, email: [email protected]
Keywords: C23, p53, tumorigenesis
Received: February 03, 2016 Accepted: July 18, 2016 Published: August 05, 2016
ABSTRACT
C23 is an abundant and multi-functional protein, which plays an important role in various biological processes, including ribosome biogenesis and maturation, cell cycle checkpoints and transcriptional regulation [1, 2]. However, the role of C23 in controlling tumorigenesis has not been well defined. Here we report that C23 is highly expressed in cancer cells and the elevated expression of C23 facilitates cancer cell proliferation in vitro and tumor xenograft growth in vivo. Notably, C23 binds to p53 through its GAR domain and suppresses the transcriptional activity of p53 under DNA damage and hypoxia. Moreover, the GAR domain is critical for C23-mediated tumor cell proliferation both in vitro and in vivo. Our findings reveal a novel role of C23 in tumorigenesis and suggest that C23 may represent a potential therapeutic target for treating malignancy.
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