The effects of the Wnt/β‑catenin signaling pathway on apoptosis in HeLa cells induced by carbon ion irradiation

The molecular mechanisms underlying the biological effects of carbon ions are unclear. The aim of this study was to explore the Wnt/betacatenin pathway in regulating carbon ion (12C6+) radiationinduced cellular toxicity. HLY78 is a Wntspecific small molecular modulator, whose effects on 12C6+ radiationinduced damage are mostly unknown. HLY78, in combination with 12C6+ radiation was investigated on HeLa cell viability, cell cycle progression, DNA damage, and the expression of apoptotic and Wntrelated proteins. 12C6+ radiation suppressed cell viability in a timedependent manner, whereas the addition of HLY78 to cells significantly reduced this stress. Moreover, after irradiation with 12C6+, HeLa cells exhibited increased cell apoptosis, G2/M phase arrest, and a number of gammaH2AX foci. However, Wnt signaling activation alleviated these effects. Furthermore, when compared with the radiation alone group, supplementation with HLY78 markedly increased the expression of antiapoptotic and Wntrelated proteins, and significantly decreased the expression of apoptotic proteins. The present results indicated that activation of the Wnt/betacatenin signaling pathway by HLY78 reduced 12C6+ radiationinduced HeLa cell dysfunction, suggesting that the Wnt/betacatenin signaling pathway plays an important role in regulating 12C6+ radiationinduced cellular toxicity in HeLa cells.