Abstract：Objective: To investigate the effect of miR-1231 on meningioma cell proliferation by targeting the EGFR /PI3K /AKT pathway. Methods: Bioinformatics software and luciferase reporter gene experiments were used to analyze and verify the targeted binding between miR-1231 and EGFR. RT-PCR was used to detect miR-1231 expression and EGFR mRNA expression in meningiomas cells. Western blot was used to detect EGFR protein expression, PI3K and AKT phosphorylation levels; CCK-8 was used to detect meningioma cell viability; colony formation assay and EdU assay was used to detect meningioma cell proliferation. Results: Compared with normal meningeal cells, the expression of miR-1231 in meningiomas cells was significantly down-regulated (P<0.05), and the expression of EGFR was significantly up-regulated (P<0.05). EGFR was confirmed as a target gene of miR-1231. Compared with miR-NC group, miR-1231 significantly inhibited meningiomas cell proliferation and inhibited EGFR/PI3K/AKT pathway (P<0.05). Compared with anti-miR-NC group, anti- miR-1231 significantly promotes meningioma cell proliferation and activates the EGFR /PI3K /AKT pathway (P<0.05). Compared with miR-NC + EGFR-NC group, miR-1231 + EGFR-NC significantly inhibits meningiomas cells EGFR /PI3K /AKT pathway (P<0.05), significantly reduced cell proliferation (P<0.05). Compared with miR-NC + EGFR-NC group, miR-NC + EGFR significantly activated meningiomas cells PI3K /AKT pathway (P<0.05) ), significantly increased cell proliferation ability (P<0.05), and could significantly reverse the inhibitory effects of miR-1231 + EGFR-NC on PI3K /AKT pathway and cell proliferation ability of meningiomas cells. Conclusion: MiR-1231 can inhibit the proliferation of meningioma cells by targeting the EGFR to regulate the PI3K /AKT pathway.
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2020, Vol. 26 
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