Abstract

Objective To investigate the effects and mechanisms of sinomenine hydrochloride (SH) on prolife ration, migration and invasion of pancreatic cancer cells. Methods Pancreatic cancer CFPAC-1 and PANC-1 cell lines were divided into three groups. The cells not treated with SH were used as a control group, and the cells treated with 0.50 mmol/L and 0.25 mmol/L of SH were used as experimental groups. The effect of cell counting kit-8 (CCK-8) and colony formation assay on cell proliferation ability was examined. The effects of wound healing and Transwell assays on cell migration and invasion. Western blotting was used to detect epithelial-mesenchymal transition (EMT)-associated protein epithelial cadherin (E-cad), neuro-cadherin (N-cad) and Vimentin (Vim). Expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 proteins in the MMPs family. Results In CCK-8 assay, SH inhibited the proliferation of cells in the 0.50 mmol/L group and 0.25 mmol/L group of CFPAC-1 and PANC-1 cells at 24 h and 48 h, and the inhibition rate were (23.97±3.31)% vs. (11.35±3.06)%, t=2.796, P<0.05; (31.62±3.30)% vs. (15.71±3.12)%, t=3.496, P<0.05; (36.09±3.64)% vs. (20.96±3.58)%, t=2.949, P<0.05; (44.80±3.90)% vs. (20.65 ± 3.53)%, t=4.586, P<0.05. The number of colonies in the CFPPAC-1 and PANC-1 0.50 mmol/L groups and the 0.25 mmol/L group were lower than those in the blank control group (13.67±0.88 vs. 49.33±2.33, t=14.300, P<0.01, 23.33±4.91). The ratio was 96.67±8.82, t=7.291, P<0.01, 28.00±1.15 to 49.33±2.33, t=8.194, P<0.01, 50.67±5.21 to 96.67±8.82, t=4.427, P<0.05. The wound healing rate of CFPPAC-1 and PANC-1 in 0.50 mmol/L group and 0.25 mmol/L group was lower than that in the blank control group [(25.33±1.63)% vs. (60.08±1.65)%, t=14.930, P<0.01, (37.55±2.69)% vs. (79.01±2.26)%, t=11.813, P<0.01, (42.49±2.05)% vs. (60.08±1.65)%, t=6.679, P<0.01, (51.67±2.36)% vs. (79.01±2.26)%, t=8.354, P<0.01]. Transwell test CFPPAC-1 and PANC-1 0.50 mmol/L , 0.25 mmol/L group were lower than the blank control group [(44.33±4.48) cells vs. (122.30±5.04) cells, t=11.561, P<0.01, (61.67±7.26) cells vs. (172.70±3.71) cells, t=13.610, P<0.01, (80.33±3.93) cells vs. (122.30±5.04) cells, t=6.568, P<0.01, (96.67±8.81) cells vs. (172.70±3.71) cells, t=7.943, P<0.01]. The expression levels of N-cad, Vim, MMP-2 and MMP-9 proteins in Western blotting assays were significantly decreased, while the protein expression levels of E-cad were increased. These changes showed a concentration-dependent relationship with SH. Conclusion SH can inhibit the proliferation, migration and invasion of pancreatic cancer CFPAC-1 and PANC-1 cells by inhibiting EMT. Key words: Pancreatic cancer; Sinomenine hydrochloride; Proliferation; Migration; Invasion; Epithelial-mesenchymal transition

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