Trichosanthin reduces the viability of SU‑DHL‑2 cells via the activation of the extrinsic and intrinsic apoptotic pathways.

Previous studies have indicated that trichosanthin (TCS) exerts antitumor activity by inducing apoptosis in numerous tumor cell lines. However, the effects of TCS on lymphoma remain to be elucidated. The current study demonstrated that TCS inhibited the proliferation of thirteen lymphoma cell lines in a dose‑dependent manner, with SU‑DHL‑2 cells exhibiting the greatest sensitivity to TCS. Treatment of SU‑DHL‑2 cells with TCS led to cell cycle arrest at the S to G2/M phase transition. Furthermore, flow cytometric analysis, Hoechst 33258 staining and western blotting indicated that TCS induced the apoptosis of SU‑DHL‑2 cells in a time‑ and concentration‑dependent manner. In addition, the activation of caspase‑3 and ‑7 and poly (ADP‑ribose) polymerase were observed. Pharmacological pan-caspase inhibition was observed to reduce TCS‑induced apoptosis. Inhibition of caspase‑8 or ‑9 alone was observed to partially reverse the effect of TCS on apoptosis. In conclusion, the current study indicates that TCS may induce apoptosis in SU‑DHL‑2 cells via the extrinsic and intrinsic pathways.