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微小RNA-592靶向胰岛素样生长因子-1受体以抑制肝细胞癌的细胞增殖、迁移和侵袭。

MicroRNA-592 targets IGF-1R to suppress cellular proliferation, migration and invasion in hepatocellular carcinoma.

作者信息

Wang Wenyao, Zhang Hongfei, Tang Mao, Liu Longlong, Zhou Zhengfang, Zhang Shaojun, Wang Lichao

机构信息

Department of General Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.

出版信息

Oncol Lett. 2017 May;13(5):3522-3528. doi: 10.3892/ol.2017.5902. Epub 2017 Mar 24.

DOI:10.3892/ol.2017.5902
PMID:28529580
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5431753/
Abstract

MicroRNAs (miRs) can function as tumor suppressors or oncogenes in different types of human malignancy, and may provide an effective therapy for cancer. The expression and functions of miR-592 have previously been studied in relation to cancer. However, the expression and potential functions of miR-592 in hepatocellular carcinoma (HCC) are still unknown. Using quantitative polymerase chain reaction, MTT assays, cellular migration and invasion assays, bioinformatics software, western blot analysis and dual-luciferase report assays, the present study explored the expression and roles of miR-592 in HCC. It was identified that miR-592 was significantly downregulated in HCC tissues and cell lines. The statistical analysis revealed that low expression of miR-592 was evidently associated with tumor node metastasis stage and lymph node metastasis. Additionally, the present study provided the first evidence that miR-592 was likely to directly target the insulin-like growth factor 1 receptor . The present results indicated that miR-592 could be investigated as an efficacious therapeutic target for HCC in the future.

摘要

微小RNA(miR)在不同类型的人类恶性肿瘤中可发挥肿瘤抑制因子或癌基因的作用,并可能为癌症提供有效的治疗方法。此前已针对癌症研究了miR-592的表达和功能。然而,miR-592在肝细胞癌(HCC)中的表达及潜在功能仍不清楚。本研究采用定量聚合酶链反应、MTT法、细胞迁移和侵袭试验、生物信息学软件、蛋白质印迹分析及双荧光素酶报告基因检测,探讨了miR-592在HCC中的表达及作用。研究发现,miR-592在HCC组织和细胞系中显著下调。统计分析显示,miR-592低表达明显与肿瘤结节转移分期及淋巴结转移相关。此外,本研究首次提供证据表明,miR-592可能直接靶向胰岛素样生长因子1受体。目前结果表明,miR-592未来有望作为HCC的有效治疗靶点进行研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/e743c34ee36f/ol-13-05-3522-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/fc6e517810c7/ol-13-05-3522-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/ff60dd35ec58/ol-13-05-3522-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/55449a57f234/ol-13-05-3522-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/049a841de153/ol-13-05-3522-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/4d7948a8cde4/ol-13-05-3522-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/e743c34ee36f/ol-13-05-3522-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/fc6e517810c7/ol-13-05-3522-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/ff60dd35ec58/ol-13-05-3522-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/55449a57f234/ol-13-05-3522-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/049a841de153/ol-13-05-3522-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/4d7948a8cde4/ol-13-05-3522-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/505d/5431753/e743c34ee36f/ol-13-05-3522-g05.jpg

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