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Ring finger protein 19A is overexpressed in non-small cell lung cancer and mediates p53 ubiquitin-degradation to promote cancer growth |
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| Authors: | Yu Cheng Yujiao Hu Huanxi Wang Zhi Zhao Xizi Jiang Yao Zhang Jiameng Zhang Yue Tong Xueshan Qiu |
| Institution: | 1. Department of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China;2. Department of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China
Contribution: Methodology (equal);3. Department of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China Contribution: Data curation (equal), Methodology (equal);4. Department of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China Department of Pathology, Zhengzhou Yihe Hospital Affiliated to Henan University, Zhengzhou, China Contribution: Data curation (equal), Methodology (equal), Software (equal);5. Department of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China Contribution: Data curation (equal), Methodology (equal), Software (equal);6. Department of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China Contribution: Methodology (equal), Resources (equal) |
| Abstract: | The expression pattern, biological functions and the related mechanisms of the ring finger protein 19A (RNF19A) in non-small cell lung cancer (NSCLC) remain poorly understood. This study aimed to explore the role of RNF19A, as well as the underlying potential mechanism, in the development of NSCLC. Here, we found that RNF19A was overexpressed in NSCLC tissues, and RNF19A expression in NSCLC tissue samples was associated with NSCLC carcinogenesis and poor outcome. RNF19A promoted the proliferation of NSCLC cells and inhibited apoptosis. RNF19A reduced p53, p21 and BAX expression and induced Cyclin D1, CDK4, CDK6 and BCL2 expression. The inhibitory effect of RNF19A knockdown on proliferation was partially rescued by p53 silencing. RNF19A interacted with p53, shortened p53 half-life and mediated p53 ubiquitin-degradation. Collectively, we suggest that RNF19A plays a critical oncogenic role in lung carcinogenesis by disrupting the function of p53. RNF19A may serve as a new biomarker and/or target for NSCLC management. |
| Keywords: | carcinogenesis non-small cell lung cancer p53 RNF19A ubiquitin |