| Literature DB >> 32142853 |
Shuang Pan1, Fu Ren2, Lei Li3, Dahua Liu4, Yao Li1, Aimei Wang1, Weihong Li1, Yongyan Dong5, Wenjuan Guo6.
Abstract
MiR-328-3p has been reported to be downregulated and serve as a tumor suppressor in several cancers. Previous studies only have reported the downregulation of miR-328-3p in CRC. However, the roles of miR-328-3p in CRC growth and metastasis were unknown. In this study, we demonstrated that miR-328-3p overexpression inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). The PI3K/Akt signaling pathway was also inactivated by miR-328-3p overexpression. MiR-328-3p knockdown showed the opposite effects. In addition, we confirmed that miR-328-3p directly bound to 3'UTR of Girdin and negatively regulated its expression. Girdin knockdown or treatment with PI3K inhibitor LY294002 blocked the effects of miR-328-3p inhibitor on cell proliferation, metastasis, and the PI3K/Akt signaling pathway. Moreover, pre-miR-328 decreased numbers of liver metastatic nodules, and reduced the levels of p-Akt, p-Girdin, and Girdin in metastatic tissues in liver. In conclusion, miR-328-3p may inhibit proliferation and metastasis of CRC cells by targeting Girdin and inactivating the PI3K/Akt signaling pathway. MiR-328-3p may be a novel target in cancer therapy.Entities:
Keywords: Colorectal cancer; Girdin; Metastasis; PI3K/Akt; miR-328–3p
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Year: 2020 PMID: 32142853 DOI: 10.1016/j.yexcr.2020.111939
Source DB: PubMed Journal: Exp Cell Res ISSN: 0014-4827 Impact factor: 3.905