Abstract：Objective: To explore the roles of emodin on proliferation, migration and invasion of pancreatic cancer SW1990 cells and its molecular mechanism. Methods: Human pancreatic ductal epithelial cells HPDE6 and pancreatic cancer SW1990 cells were cultured in vitro, and SW1990 cells were divided into control group, low-dose emodin group, medium-dose emodin group, high-dose emodin group, miR-NC group, miR-1301 group, high-dose emodin+anti-miR-NC group, high-dose emodin+anti-miR-1301 group. Real-time fluorescence quantitative PCR (RT-qPCR) was used to detect the expressions of miR-1301. The tetramethylazozolate colorimetric method (MTT) was implemented to measure cell activity. The protein expression was assessed by Western blot. Transwell was employed to monitor cell migration and invasion. Results: Compared with human pancreatic ductal epithelial cells HPDE6, the expression level of miR-1301 in pancreatic cancer SW1990 cells was significantly decreased(P<0.05). Compared with the control group, medium and high-doses of emodin significantly decreased the activity, migration and invasion ability and the levels of CyclinD1, MMP-2 and MMP-9, and increased the level of p21 of pancreatic cancer SW1990 cells(P<0.05). Compared with the control group, the expression levels of miR-1301 in medium and high-dose emodin groups were significantly increased(P<0.05). Overexpression of miR-1301 significantly reduced the activity, migration and invasion ability and the levels of CyclinD1, MMP-2 and MMP-9, and increased the level of p21 of pancreatic cancer SW1990 cells(P<0.05). Down-regulation of miR-1301 reversed the roles of emodin on proliferation, migration and invasion of pancreatic cancer SW1990 cells(P<0.05). Conclusion: Emodin may inhibit cell proliferation, migration and invasion by up-regulating the expression of miR-1301 in SW1990 cells.
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2022, Vol. 28 
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