miR-133a, directly targeted USP39, suppresses cell proliferation and predicts prognosis of gastric cancer.
miR-133a, directly targeted USP39, suppresses cell proliferation and predicts prognosis of gastric cancer.
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DOI：
10.3892/ol.2018.8421
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发表时间：
2018-06
期刊：
影响因子：
2.9
通讯作者：
Fan L
中科院分区：
文献类型：
--
作者：
Dong X;Su H;Jiang F;Li H;Shi G;Fan L
胃癌发病率和死亡率都很高，仅次于肺癌居第二位。在某些类型的肿瘤中已经观察到miR-133 a的下调，并且其参与胃癌。本研究旨在探讨miR-133 a和泛素特异性蛋白酶39（USP 39）在胃癌中的作用机制。采用Western blot和RT-PCR检测miR-133 a和USP 39的表达。为了确认miR-133 a是否靶向USP 39，我们进行了荧光素酶报告基因测定。采用MTT法检测miR-133 a对胃癌细胞增殖的影响。miR-133 a在癌组织和细胞系（HGC-27和MGC-803）中表达显著下调，而USP 39在肿瘤组织中的表达水平高于癌旁组织。上调miR-133 a表达和/或下调USP 39表达可抑制胃癌细胞的增殖。此外，USP 39被确定为miR-133 a的直接靶点，并且还观察到它们之间的负相关关系。USP 39是miR-133 a的第一手靶点，两者之间呈负相关。此外，miR-133 a的低表达或USP 39的过表达预测不良预后。总之，miR-133 a可能是microRNA介导的CC细胞增殖抑制的新治疗靶点，但miR-133 a/USP 39轴在CC进展中的作用需要进一步研究。
Gastric cancer has high incidence and mortality, and the mortality ranks second only to lung cancer. Downregulation of miR-133a has been observed in certain types of tumors, and it is involved in gastric cancer. The aim of the present study was to explore the molecular mechanisms of miR-133a and ubiquitin-specific protease 39 (USP39) in gastric cancer. Western blot analysis and RT-PCR were employed to measure miR-133a and USP39 expression. To confirm whether miR-133a targeted USP39, we conducted a luciferase reporter assay. We utilized 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay to detect the effects of miR-133a on gastric cell proliferation. miR-133a was significantly downregulated in cancer tissues and cell lines (HGC-27 and MGC-803), while the expression level of USP39 was higher in tumor tissues than in paracancerous tissues. Upregulated expression of miR-133a and/or USP39 downregulation could inhibit cell proliferation in gastric cancer cells. Furthermore, USP39 was identified as a direct target of miR-133a and the inverse relationship between them was also observed. USP39 was a firsthand target of miR-133a and there was a negative correlation between them. In addition, a low expression of miR-133a or overexpression of USP39 predicted poor prognosis. In conclusion, miR-133a may be a novel therapeutic target of microRNA-mediated suppression of cell proliferation in CC, but the role of the miR-133a/USP39 axis in CC progression needs further study.
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