Abstract

To explore the role of dihydromyricetin (DHM) in regulating proliferation, metastasis and infiltration of pancreatic cancer cells, we treated the pancreatic adenocarcinoma cell line SW1990 with 10 µmol/L, 20 µmol/L, and 40 µmol/L DHM. Proliferation was determined by the MTT assay. Cell metastasis and infiltration were determined by the Transwell migration assay. The protein expression levels of cyclin D1, p21, MMP-2, MMP-9, and PRMT5 were determined by Western blot. Quantitative PCR was used to determine expression of miR-509-3p and PRMT5 mRNA. The relationship between miR-509-3p and PRMT5 was analyzed by bioinformatic prediction and the dual luciferase reporter assay. SW1990 cells were transfected with miR-509-3p, si-PRMT5 and anti-miR-509-3p (following treatment with 40 µmol/L DHM) to determine their effects on biological behaviors of cells. The inhibition rate of SW1990 cells, p21 protein and miR-509-3p expression were increased by DHM. Moreover, the number of infiltrating and metastatic cells, protein levels of cyclin D1, MMP-2, MMP-9, and PRMT5, and mRNA levels of PRMT5 were decreased by DHM. miR-509-3p regulates expression of its target PRMT5 mRNA. Inhibition rate of SW1990 cell proliferation and protein level p21 were significantly increased by overexpression of miR-509-3p or knockdown of PRMT5 expression, while the number of invasive cells and protein expression levels of cyclin D1, MMP-2 and MMP-9 were remarkably reduced by miR-509-3p overexpression or PRMT5 knockdown. Inhibition of miR-509-3p counteract the inhibitory effects of DHM on SW1990 cell proliferation and metastasis. Therefore, DHM inhibits proliferation and metastasis of pancreatic carcinoma cells by regulating the miR-509-3p/PRMT5 pathway.

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