Upregulation of Myc promotes the evasion of NK cell‑mediated immunity through suppression of NKG2D ligands in K562 cells.

c‑Myc is a characteristic oncogene with dual functions in cell proliferation and apoptosis. Since the overexpression of the c‑Myc proto‑oncogene is a common event in the development and growth of various human types of cancer, the present study investigated whether oncogenic c‑Myc can alter natural killer (NK) cell‑mediated immunity through the expression of associated genes, using PCR, western blotting and flow cytometry assays. Furthermore, whether c‑Myc could influence the expression levels of natural killer group 2 member D (NKG2D) ligands, which are well known NK activation molecules, as well as NK cell‑mediated immunity, was investigated. c‑Myc was inhibited by 10058‑F4 treatment and small interfering RNA transfection. Upregulation of c‑Myc was achieved by transfection with a pCMV6‑myc vector. The inhibition of c‑Myc increased MHC class I polyeptide‑related sequence B and UL16 binding protein 1 expressions among NKG2D ligands, and the overexpression of c‑Myc suppressed the expression of all NKG2D ligands, except MHC class I polyeptide‑related sequence A. Furthermore, the alteration of c‑Myc activity altered the susceptibility of K562 cells to NK cells. These results suggested that the overexpression of c‑Myc may contribute to the immune escape of cancer cells and cell proliferation. Combined treatment with NK‑based cancer immunotherapy and inhibition of c‑Myc may achieve improved therapeutic results.