Experimental study of the role of dalteparin sodium in inhibiting the proliferation of human lung adenocarcinoma cell

Objective:To investigate the mechanism of dalteparin in inhibiting the human lung adenocarcinoma cell proliferation． Methods:The cycle changes of A549 cells after dalteparin treatment were detected by flow cytometry． After the mouse models of lung cancer were established，the 12 tumor-bearing mice were randomly divided into dalteparin group and control group;they were given 1 500 IU/kg(0． 2 ml) subcutaneously or 0． 9% chloride sodium intraperitoneally(0． 2 ml) once a day for 35 days． The maximum diameter and the minimum diameter of the tumor were measured regularly;the tumor volume was calculated and the tumor growth curve was made． Thirty-five days later，the mice were executed after anesthetized with amyl phenobarbital sodium． The tumor was stripped and weighed，the inhibitory rate was calculated and the expression of Cyclin E in tumor tissue was measured using immunohistochemical method． Results:Forty-eight hours after the lung adenocarcinoma cell line A549 was treated，the proportion of cells in G0/G1phase were increased and S phase were decreased in the dalteparin group compared with that of the control group(P 0． 01);the tumor weight in the dalteparin group was significantly reduced compared with that in the control group(P 0． 05);the tumor inhibition rate in the dalteparin group was 64． 081%． The positive expression of Cyclin E was 6/6 and 3/6 respectively in the dalteparin group and the control group;the difference was not statistically significant(P = 0． 182)． The dalteparin group mainly showed low expression(5/6)， while the control group showed high expression(5/6);the difference was not statistically significant(P = 0． 081)． Conclusions: Dalteparin can block human lung adenocarcinoma A549 cells in G0/G1phase，the cell entry into S phase and M phase is reduced，the DNA synthesis is decreased and the cell proliferation is inhibited，which might be related to the expression of inhibiting cell cycle regulator Cyclin E．