MicroRNA-32 (miR-32) regulates phosphatase and tensin homologue (PTEN) expression and promotes growth, migration, and invasion in colorectal carcinoma cells.
MicroRNA-32 (miR-32) regulates phosphatase and tensin homologue (PTEN) expression and promotes growth, migration, and invasion in colorectal carcinoma cells.
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DOI：
10.1186/1476-4598-12-30
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发表时间：
2013-04-23
期刊：
影响因子：
37.3
通讯作者：
Zhou Y
中科院分区：
文献类型：
--
作者：
Wu W;Yang J;Feng X;Wang H;Ye S;Yang P;Tan W;Wei G;Zhou Y
结直肠癌（CRC）是全球癌症相关死亡的主要原因之一。 MicroRNA（miRNA、miR）在癌发生过程中发挥着重要作用。 MiR-32 已被证明在 CRC 中表达上调。在本研究中，我们鉴定了miR-32对CRC细胞一些重要生物学特性的潜在影响，并阐明了miR-32对PTEN的调控。使用 miR-32 模拟物/抑制剂来增加/减少 miR-32 表达，在 CRC 细胞系中评估 miR-32 对 PTEN 表达的影响。此外，用 miR-32 模拟物/抑制剂转染细胞分析了 miR-32 在调节 CRC 细胞生物学特性中的作用。通过双荧光素酶报告基因测定验证 PTEN 的 3'-非翻译区 (3'-UTR) 与 miR-32 的结合。功能获得和功能丧失研究表明，miR-32 的过表达促进 SW480 细胞增殖、迁移和侵袭，减少细胞凋亡，并导致转录后水平 PTEN 下调。然而，miR-32 敲除抑制了 HCT-116 细胞中的这些过程并增强了 PTEN 蛋白的表达。此外，我们通过直接靶向PTEN的3'-UTR，进一步确定PTEN是miR-32的功能性下游靶点。我们的结果表明，miR-32 至少部分通过抑制 PTEN 参与 CRC 的肿瘤发生。
Colorectal carcinoma (CRC) is one of the leading causes of cancer-related mortality worldwide. MicroRNAs (miRNAs, miRs) play important roles in carcinogenesis. MiR-32 has been shown to be upregulated in CRC. In this study, we identified the potential effects of miR-32 on some important biological properties of CRC cells, and clarified the regulation of PTEN by miR-32. The effect of miR-32 on PTEN expression was assessed in CRC cell lines with miR-32 mimics/inhibitor to increase/decrease miR-32 expression. Furthermore, the roles of miR-32 in regulating CRC cells biological properties were analyzed with miR-32 mimics/inhibitor-transfected cells. The 3′-untranslated region (3′-UTR) of PTEN combined with miR-32 was verified by dual-luciferase reporter assay. Gain-of-function and loss-of-function studies showed that overexpression of miR-32 promoted SW480 cell proliferation, migration, and invasion, reduced apoptosis, and resulted in downregulation of PTEN at a posttranscriptional level. However, miR-32 knock-down inhibited these processes in HCT-116 cells and enhanced the expression of PTEN protein. In addition, we further identified PTEN as the functional downstream target of miR-32 by directly targeting the 3′-UTR of PTEN. Our results demonstrated that miR-32 was involved in tumorigenesis of CRC at least in part by suppression of PTEN.
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