title: Trichosanthin reduces the viability of SU‑DHL‑2 cells via the activation of the extrinsic and intrinsic apoptotic pathways.
abstract: 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.
authors.affiliation: State Key Laboratory of Oncology in Southern China, Collaborative Innovation Center for Cancer Medicine, Sun Yat‑sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.
authors.forename: Yingjie
authors.initials: Y
authors.lastname: Zhu
authors.affiliation: Department of Thoracic Oncology, Guangdong Lung Cancer Institute, Guangdong General Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
authors.forename: Yueli
authors.initials: Y
authors.lastname: Sun
authors.affiliation: State Key Laboratory of Oncology in Southern China, Collaborative Innovation Center for Cancer Medicine, Sun Yat‑sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.
authors.forename: Yuchen
authors.initials: Y
authors.lastname: Cai
authors.affiliation: Department of Basic Medical Sciences, School of Medicine, Shenzhen University, Shenzhen, Guangdong 518060, P.R. China.
authors.forename: Ou
authors.initials: O
authors.lastname: Sha
authors.affiliation: State Key Laboratory of Oncology in Southern China, Collaborative Innovation Center for Cancer Medicine, Sun Yat‑sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.
authors.forename: Wenqi
authors.initials: W
authors.lastname: Jiang
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000378:metabolism; D059447:Cell Cycle Checkpoints / Q000187:drug effects; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004591:Electrophoresis, Polyacrylamide Gel; D006801:Humans; D008223:Lymphoma / Q000473:pathology; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013997:Time Factors; D015978:Trichosanthin / Q000494:pharmacology*
chemical_list: D015978:Trichosanthin; D011065:Poly(ADP-ribose) Polymerases; D020169:Caspases