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首页> 外文期刊>Molecular Cancer >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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MicroRNA-32 (miR-32) regulates phosphatase and tensin homologue (PTEN) expression and promotes growth, migration, and invasion in colorectal carcinoma cells

机译：MicroRNA-32（miR-32）调节磷酸酶和张力蛋白同源物（PTEN）的表达，并促进结直肠癌细胞的生长，迁移和侵袭

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Background 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. Methods 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. Results 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 . Conclusions Our results demonstrated that miR-32 was involved in tumorigenesis of CRC at least in part by suppression of PTEN .
机译：背景大肠癌（CRC）是全球范围内与癌症相关的死亡率的主要原因之一。微小RNA（miRNA，miRs）在癌变过程中起重要作用。已证明MiR-32在CRC中上调。在这项研究中，我们确定了miR-32对CRC细胞某些重要生物学特性的潜在影响，并阐明了miR-32对PTEN的调控。方法在具有miR-32模拟物/抑制剂以增加/减少miR-32表达的CRC细胞系中评估miR-32对PTEN表达的影响。此外，用miR-32模拟物/抑制剂转染的细胞分析了miR-32在调节CRC细胞生物学特性中的作用。 PTEN与miR-结合的3 '-非翻译区（3 ' -UTR）通过双重萤光素酶报告基因分析证实了32个。结果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，减少凋亡，并导致转录后水平PTEN的下调。但是，miR-32敲低抑制了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，进一步将PTEN鉴定为miR-32的功能性下游靶标。结论我们的结果表明miR-32至少部分通过抑制PTEN参与了CRC的肿瘤发生。

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