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Aim The study was conducted to investigate the role of c-Myc in the regulation of ionizing radiation-induced cell cycle arrest and cell death in human cervical cancer cells. Methods Control and c-Myc-silenced Hela cells were collected at different time points after 60Co γ-ray radiation. Flow cytometry was used to measure cell cycle distribution and apoptosis. Immunofluorescence was applied to determine the percentage of cells in M phase. Transmission electron microscopy and immunoblotting were used to detect the induction of autophagy after radiation. Immunoblotting was also used to measure the expression levels of apoptosis-related proteins. Results In c-Myc-silenced cells, radiation induced delayed but long-lasting G2/M arrest and an abnormal M phase compared with the control. In addition, c-Myc knockdown significantly inhibited apoptotic cell death induced by radiation. Meanwhile, radiation-induced autophagy appeared stronger in c-Myc-silenced cells. Mechanically, we found that Caspase 8 and survivin expression was decreased in c-Myc-silenced Hela-630 cells. Conclusions These data showed that c-Myc serves as a co-regulator in radiation-induced G2/M cell cycle arrest and cell death in human cervical cancer cells. [ABSTRACT FROM AUTHOR]