MiR-328-3p inhibits cell proliferation and metastasis in colorectal cancer by targeting Girdin and inhibiting the PI3K/Akt signaling pathway

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. •MiR-328–3p inhibited cell proliferation and metastasis via Girdin and the PI3K/Akt pathway.•MiR-328–3p knockdown showed the opposite effects.•Girdin is a direct target of miR-328–3p.•Pre-miR-328 suppressed CRC liver metastasis in vivo.