MiR-335 acts as a potential tumor suppressor miRNA via downregulating ROCK1 expression in hepatocellular carcinoma (Retracted article. See April, 2017)
MiR-335 acts as a potential tumor suppressor miRNA via downregulating ROCK1 expression in hepatocellular carcinoma (Retracted article. See April, 2017)
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DOI：
10.1007/s13277-015-3317-2
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发表时间：
2015-08-01
期刊：
影响因子：
--
通讯作者：
Long, Xueying
中科院分区：
文献类型：
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作者：
Liu, Hui;Li, Wenzheng;Long, Xueying
越来越多的证据表明，microRNAs（miRNAs）的失调可能有助于肿瘤的进展。先前的miRNA微阵列分析表明，miR-335在各种癌症中下调;然而，miR-335在肝细胞癌（HCC）中的作用尚未得到很好的阐明。本研究旨在探讨miR-335在体外人肝癌中的生物学功能和分子机制，探讨其是否可能成为肝癌治疗的生物标志物。通过定量RT-PCR分析了4种HCC细胞系和62例HCC患者的样本中miR-335的表达。通过将模拟物转染到HepG 2和HuH 7细胞中来建立miR-335的过表达。通过细胞活力测定和transwell法检测细胞增殖和迁移。荧光素酶报告基因检测和Western blot检测证实ROCK 1为miR-335的新靶基因。我们观察到miR-335在人HCC组织和所有四种HCC细胞系中下调。MTT分析显示miR-335的过表达随后抑制细胞生长。此外，transwell测定还显示miR-335转染子中的显著细胞迁移抑制。过表达miR-335后，ROCK 1的表达明显降低，表明ROCK 1是miR-335的靶基因。我们的数据显示，miR-335可以通过调控ROCK 1抑制肝癌细胞的增殖和迁移侵袭，提示miR-335有可能成为肝癌治疗的生物标志物。
Increasing evidence has suggested that dysregulation of microRNAs (miRNAs) could contribute to tumor progression. Previous miRNA microarray analysis illustrated that miR-335 is downregulated in various cancers; however, the role of miR-335 on hepatocellular carcinoma (HCC) has not been well elucidated. In this study, we investigated the biological functions and molecular mechanisms of miR-335 in human HCC in vitro, discussing whether it could be a therapeutic biomarker of HCC in the future. Four HCC cell lines and samples from 62 patients with HCC were analyzed for the expression of miR-335 by quantitative RT-PCR. Overexpression of miR-335 was established by transfecting mimics into HepG2 and HuH7 cells. Cell proliferation and cell migration were assessed by cell viability assay and transwell assay. Luciferase reporter assay and Western blot were to verify ROCK1 as a novel target gene of miR-335. We observed that miR-335 was downregulated in human HCC tissues and in all four HCC cell lines. The MTT assay revealed that overexpression of miR-335 subsequently inhibited cell growth. Furthermore, the transwell assay also showed significant cell migration inhibition in miR-335 transfectant. The expression of ROCK1 was decreased evidently after overexpression of miR-335, indicating that ROCK1 is a target gene for miR-335. Our data revealed that miR-335 could inhibit the proliferation and migration invasion of HCC cells via regulating ROCK1, suggesting that miR-335 could be a therapeutic biomarker of HCC in the future.