bjective; To investigate the effect of myocardial cells culture medium (CMCM) on the proliferation of human nasopharyngeal carcinoma cells CNE-2and to reveal its mechanism. Methods:The survival cells of human nasopharyngeal carcinoma cells CNE-2treated with CMCM for12h,24h,36h,48h,60h,72h were determined by MTT respectively; CNE-2cells treated with DDP and RPMI1640as controls. The cell-DNA ploidy distribution and apoptosis rate were measured by flow Cytometry (FCM) after cells were treated for24h and48h. Result:CMCM inhibited the growth of CNE-2cells in a time-dependent manner. At12h cell viability rate after treated with CMCM was87.27±6.99%, which is lower than control group (P<0.05). The maximal inhibitory rate was at72h.There were no statistical difference between DDP group and CMCM group before48h. Each group was detected cell cycle distribution and apoptosis with flow cytometry at24and48hours after treatment. At24h the proportion of cells in G0/G1phase of the CMCM group was64.20±2.31%while control group was52.70±1.78%.There was statistical difference (p<0.05); G2/M phase cells of the CMCM group was10.20±1.46%while control groups was4.83±0.75%,there was statistical difference (p<0.05), G2/M phase arrest of CNE-2cell of the CMCM group was less effective than cisplatin group (19.50±2.35)%(p<0.05). At48h the proportion of cells in G0/G1phase of the CMCM group was65.27±1.06%while control group was52.20±3.70%%and There was statistical difference (p <0.05); G2/M phase cells of the CMCM group was14.07±1.74%while control groups was4.47±0.83%,and there was statistical difference (p<0.05), G2/M phase arrest of CNE-2cell of the CMCM group was less effective than cisplatin group (22.87±1.15)%(p<0.05). The proportion of cells in G0/G1phase of CMCM group at24and48hours was64.20±2.31%,65.27±1.06%respectively, the difference was not statistically significant (p>0.05);while the proportion of G2/M phase cells was10.20±1.46%,14.07±1.74%,respectively, the difference was statistically significant (p<0.05). At24hour, the apoptosis rate of the CMCM group (37.43±1.85%) was higher than the DDP group (7.62±1.72%) and control group (0.14±09%), the differences were statistically significant (p<0.05);48hours, the apoptosis rate of the CMCM group (28.80±1.81%)was higher than the DDP group (21.93±2.46%) and control group (1.43±0.53%), the differences were statistically significant (p<0.05); The apoptosis rate of the CMCM group at24hour was37.43±1.85%while48hour was28.80±1.81%, showing percentage of apoptotic cells was significantly reduced(p<0.05). Conclusion:CMCM inhibited the growth of CNE-2cells in a time-dependent manner, possibly through inducing cell apoptosis and influencing cell cycle. |