Abstract:

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  controlgroup,2,4,8 μmo1/L^-1 icotinib  groups,p38-MAPK inhibitor SB203580(20 μmol/L^-1)   group, SB203580(20 μmol/L^-1)+4 μmo1/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 4 μmo1?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.

Key words: icotinib, salivary adenoid cystic carcinoma cells, mitogen-activated protein kinase, apoptosis