Yang Xiaoyan, Zang Jinglei, Pan Xia, Yin Jie, Xiang Qiong, Yu Jia, Gan Runliang, Lei Xiaoyong
Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan 421001, P.R. China.
Changsha Health Vocational College, Changsha, Hunan 410100, P.R. China.
Oncol Rep. 2017 Jan;37(1):563-570. doi: 10.3892/or.2016.5220. Epub 2016 Nov 7.
Hepatocellular carcinoma (HCC), a disease that is a major health care issue across the globe, includes the deviant expression of miRNAs in its development, progression, and resistance to treatment. We focused our study on miR‑503 expression and its role in HCC. miR‑503 was found in HCC tissues and cell lines using quantitative real-time PCR (RT‑qPCR). Western blot analyses and the luciferase reporter assay were used to determine the miR‑503 potential target in the HCC cells. We used MTT to analyze cell proliferation activity and noted that there was a considerable decrease of miR‑503 in HCC tissues and cell lines when measured against the controls. miR‑503 upregulation decreased expression of eukaryotic translation initiation factor 4E (EIF4E), and reduced HCC cell proliferation and sensitized HCC cells to anticancer drugs. miR‑503 overexpression hindered luciferase activity of EIF4E 3' untranslated region-based reporter construct among HepG2, BEL-7402, and SMMC-7721 cells, revealing that miR‑503 may increase sensitivity to therapies at least partially through targeting EIF4E suppression of HCC proliferation.
肝细胞癌（HCC）是一个全球性的重大医疗保健问题，其发展、进展和对治疗的抗性过程中存在微小RNA（miRNA）的异常表达。我们的研究聚焦于miR-503在HCC中的表达及其作用。采用定量实时聚合酶链反应（RT-qPCR）在HCC组织和细胞系中检测miR-503。运用蛋白质免疫印迹分析和荧光素酶报告基因检测来确定HCC细胞中miR-503的潜在靶标。我们使用MTT分析细胞增殖活性，发现与对照相比，HCC组织和细胞系中miR-503显著降低。miR-503上调降低了真核翻译起始因子4E（EIF4E）的表达，减少了HCC细胞增殖，并使HCC细胞对抗癌药物敏感。在HepG2、BEL-7402和SMMC-7721细胞中，miR-503过表达抑制了基于EIF4E 3'非翻译区的报告基因构建体的荧光素酶活性，表明miR-503可能至少部分通过靶向抑制EIF4E来增加对HCC增殖治疗的敏感性。
