The deregulation of p53 in
cancer cells is one of the important factors by which
cancer cells escape from the immune surveillance.
Cholecystokinin (CCK) has strong bioactivity in the regulation of a number of cell activities. This study tests a hypothesis that CCK interferes with p53 expression to affect the apoptotic process in
lung cancer (
tumor) cells. In this study,
tumor-bearing mice and A549 cells (a tumor cell line) were irradiated. The expression of CCK and p53 in
tumor cells was assessed with RT-qPCR and Western blotting. The binding of p300 to the promoter of p53 was evaluated by
chromatin immunoprecipitation. We observed that, with a given amount and within a given period, small doses/more sessions of irradiation markedly increased the levels of CCK in the sera and
tumor cells, which were positively correlated with the
tumor growth in mice and negatively correlated with
tumor cell apoptosis. CCK increased the levels of
histone acetyltransferase p300 and repressed the levels of nuclear factor-kB at the p53 promoter locus in
tumor cells, which suppressed the expression of p53. In conclusion, CCK plays an important role in attenuating the radiation-induced
lung cancer cell apoptosis. CCK may be a novel therapeutic target in the treatment of
lung cancers.