Panaxynol inhibited the proliferation and self-renewal of stem cells in pancreatic cancer

Abstract

Objective To investigate the influence of panaxynol on pancreatic cancer stem cells′ proliferation and self-renewal. Methods PANC1 cells were cultured in stem cell culture system to induce the formation of stem cells, and the proportion of CD133+ pancreatic cancer stem cells was detected by FCM. Cultured pancreatic stem cells were treated with panaxynol at different concentrations of 0, 72, 144, 287 nmol/L for 0, 12, 24, 48 h. CCK8 kit was used to detect the cell survival. The colony formation experiment detected the number of colonies after being cultured with 287 nmol/L panaxynol for 48 h. Western blot was used to detect the expression of proliferation-related protein Ki67, PCNA and self-renewal related protein β-catenin. Results The CD133+ proportion of pancreatic cancer stem cells was (9.70±0.59)%, which was statistically higher than that [(2.11±0.25)%] in the control group (P<0.001). Panaxynol can decrease the survival rates of pancreatic cancer stem cells in a dosage and time dependent manner. The survival rate of stem cells in control, 72, 144, 287 nmol/L panaxynol group was 100%, (63.32±2.37)%, (49.91±2.13)% and (41.37±2.01)% after cultured for 48 h, which had statistically significant difference among different groups (P<0.001). The number of colonies in the control and 287 nmol/L panaxynol group was(611±25) and(280±16). Colonies in panaxynol group were fewer than those in the control group with statistically difference(P<0.001). The expression of Ki67, PCNA and β-catenin were 0.376±0.012, 0.772±0.026 and 0.219±0.018 in the control group and were 0.183±0.010, 0.453±0.009 and 0.148±0.006 in panaxynol group, respectively. The results indicated that Ki67, PCNA and β-catenin were down-regulated by panaxynol treatment and the differences were statistically significant (P<0.01). Conclusions Panaxynol can inhibit the proliferation and self-renewal of pancreatic cancer stem cells. These effects may be related to downregulating Ki67, PCNA and blocking Wnt/β-catenin signaling pathway. Key words: Pancreatic neoplasms; Stem cells; Panaxynol; Cell proliferation