Affiliations: [a] Department of Chest Surgery, the Central Hospital of Linyi, Yishui, Shandong, China | [b] Department of Health, Linyi University Yishui, Yishui, Shandong, China | [c] Department of Radiotherapy, the Second Affiliated Hospital of Qingdao University, Qingdao, Shandong, China | [d] Department of Clinical Laboratory, Yantaishan Hospital, Yantai, Shandong, China | [e] Department of Emergency Surgery, Qingdao Medical Center, Qingdao, Shandong, China
Correspondence:
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Corresponding author: Yunxiang Shi, Department of Chest Surgery, the Central Hospital of Linyi, Yishui, Shandong, China. E-mail: yszxyysyx@126.com.
Abstract: Studies have shown that microRNAs (miRNAs) can promote or suppress tumor growth and therefore act as targets for cancer therapy. Hsa-miR-503-5p, a mature miRNA derived from 5’ ends of pre-miR-503, has been proved to regulate cell proliferation, transformation, migration and invasion. However, the biological function of miR-503-3p derived from 3’ ends of pre-miR-503 has never been reported. In current study, we found that miR-503-3p inhibits lung cancer cell viability and induces cell apoptosis. To better understand the molecular mechanism underlying the miR-503-3p participating in this process, PCR array and RNA-sequencing (RNA-seq) were performed and some differential expression genes were discovered between NC and miR-503-3p treated groups. Biological interaction network showed that p21 and CDK4 are the most important proteins involving miR-503-3p signal pathway. Dual-luciferase assay results shown miR-503-3p directly regulates the expression of p21 by targeting 3’-UTR of its mRNA. These results shed light on the potential roles of miR-503-3p, indicating that it may act as an anti-oncogene factor to inhibit lung cancer cell viability.
