Natural killer (NK) cells have received a lot of attention in recent years for the roles they play\nin immunity and particularly in antitumor immune responses. Although defects in NK cell functions\nare recognized as important mechanisms for immune evasion of malignant cells, molecular pathways\nregulating NK cell dysfunction and exhaustion in cancer are largely unknown. Here we tested\nwhether the c-myc proto-oncogene, known to promote cell proliferation, growth, differentiation, and\napoptosis by regulating the expression of numerous target genes, may be involved in the mechanism\nof NK cell abnormalities in patients with lung and gastric cancer. Analysis of c-myc mRNA and\nprotein expression in peripheral blood NK cells, mitogen-activated protein kinase (MAPK) activity,\ncell cycle, and cell longevity revealed a significantly decreased expression of c-myc mRNA and\nprotein and mitotic arrest of NK cells in different phases of cell cycle. In addition, a significant\ndecrease of NK cell death was also detected. These data allow the suggestion that defects of NK\ncell-mediated tumor surveillance may be associated with disturbed c-myc expression in NK cells in\ncancer patients. A better understanding of the mechanisms of NK cell dysfunction in cancer will help\nin the NK cell-mediated therapeutic eradication of primary and metastatic cancer cells and prolong\npatient survival.
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