RESUMO
Autophagy and apoptosis both promote cell death; however, the relationship between them is subtle, and they mutually promote and antagonize each other. Apoptin can induce apoptosis of various tumor cells; however, tumor cell death is not only caused by apoptosis. Whether apoptin affects tumor cell autophagy is poorly understood. Therefore, the present study aimed to explore the potential mechanisms underlying the effects of apoptin using recombinant adenoviruses expressing apoptin. Reverse transcriptionquantitative polymerase chain reaction, immunoblotting, flow cytometry, fluorescence microscopy and proteomics analyses revealed that apoptin could induce autophagy in MCF7 breast cancer cells. The results also suggested that apoptin affected autophagy in a time and dosedependent manner. During the early stage of apoptin stimulation (6 and 12 h), the expression levels of autophagy pathwayassociated proteins, including Beclin1, microtubuleassociated protein 1A/1Blight chain 3, autophagyrelated 4B cysteine peptidase and autophagyrelated 5, were significantly increased, suggesting that apoptin promoted the upregulation of autophagy in MCF7 cells. Conversely, after 12 h of apoptin stimulation, the expression levels of apoptosisassociated proteins were decreased, thus suggesting that apoptosis may be inhibited. Therefore, it was hypothesized that apoptin may enhance autophagy and inhibit apoptosis in MCF7 cells at the early stage. In conclusion, apoptininduced cell death may involve both autophagy and apoptosis. The induction of autophagy may inhibit apoptosis, whereas apoptosis may inhibit autophagy; however, occasionally both pathways operate at the same time and involve apoptin. This apoptinassociated selection between tumor cell survival and death may provide a potential therapeutic strategy for breast cancer.