Induction effect of icotinib on apoptosis of salivary adenoid cystic carcinoma ACC-M cells through p38-MAPK pathway / 吉林大学学报(医学版)

ABSTRACT

Objective To explore the influence of icotinib in the apoptosis of the human salivary adenoid cystic carcinoma cells ACC-M, and to clarify the mechanism of icotinib for the treatment of salivary adenoid cystic carcinoma.Methods The ACC-M cells were randomly divided into control group,2,4,8μmo1·L-1 icotinib groups,p38-MAPK inhibitor SB203580 (20μmol· L-1 )group,SB203580 (20 μmol· L-1 )+4μmo1 · L-1 icotinib group;the cells were collected 4 h after treatment.The viability of ACC-M cells was measured by MTT assay.The apoptosis of ACC-M cells was assessed by caspase-3 activity kit. The expression of p-p38-MAPK protein was determined by Western blotting analysis.Results Compared with control group,the inhibitory rates of growth of the ACC-M cells in icotinib groups were significantly decreased (P<0.05 ), and the activities of caspase-3 were increased (P<0.05),and the expression levels of p-p38-MAPK were significantly increased (P<0.05).Compared with 4μmo1·L-1 icotinib group,the expression level of p-p38-MAPK in SB203580+icotinib group were decreased (P < 0.05 ), and the activity of caspase-3 was decreased dramatically (P < 0.05 ). Conclusion Icotinib may induce the apoptosis of ACC-M cells through the activation of p38-MAPK signaling pathway.