Background and Aims: Pancreatic cancer is a highly malignant tumor of the digestive system. Although the current treatment for pancreatic cancer is constantly evolving, the prognosis of pancreatic cancer patients is still poor. Cryptotanshinone (CPT) is a monomer extracted from Chinese medicinal herb salvia miltiorrhiza with variety of activities, which has been proven to have anti-cancer potential against cervical cancer and prostate cancer, etc. However, its effect on pancreatic cancer is still unclear. This study was conducted to investigate the effect of CPT on the growth and migration of pancreatic cancer cells in vitro and the possible mechanism, so as to provide theoretical and experimental basis for the development of relevant drugs for clinical use. 
Methods: The human pancreatic cancer BxPC-3 and SW1990 cells were used as study subjects. In these two types of pancreatic cancer cells, the concentration and time effects of CPT on cell viability were determined after treatment with different concentrations (10, 20 and 40 μmol/L) of CPT for different times (0, 1, 2 and 3 d); the changes in abilities of colony formation, migration and invasion after treatment with above concentrations of CPT for 24 h were determined by colony forming assay, scratch wound healing assay and Transwell assay, respectively; the expressions of Akt, phosphorylated Akt (p-AKT), and the epithelial-mesenchymal transition (EMT)-associated proteins vimentin and E-cadherin as well as the cell cycle-related proteins CDK4, cyclin D1 after treatment with 20 μmol/L CPT for different times were determined by Western blot analysis. The cells for control were treated with the vehicle (DMSO) only.
Results: In the two types of pancreatic cancer cells compared with corresponding control group, the growth abilities were significantly inhibited after CPT treatment, with a concentration- and time-dependent manner (all P<0.05); the degree of wound healing, relative colony formation rate and number of invading cells were significantly reduced, with a concentration-dependent manner (all P<0.05); the protein expressions of Akt, p-Akt, vimentin and E-cadherin, CDK4 and cyclin D1 were all significantly down-regulated, with a time-dependent manner (all P<0.05). 
Conclusion: CPT can effectively inhibit the growth and migration of pancreatic cancer cells, and the mechanism may be probably associated with its downregulating the expression of Akt and thereby, cause the cell cycle arrest and inhibition of the EMT process of the pancreatic cancer cells.