Wei Wenwen, Zhao Xindong, Wu Shaoling, Zhao Chunting, Zhao Hongguo, Sun Lingjie, Cui Yujiao
Department of Hematology, Affiliated Hospital, Qingdao University, Qingdao, Shandong 266003, P.R. China.
Department of Hematology, School of Medicine, Qingdao University, Qingdao, Shandong 266021, P.R. China.
Oncol Lett. 2018 Nov;16(5):6838-6846. doi: 10.3892/ol.2018.9450. Epub 2018 Sep 18.
Recent studies have revealed a positive therapeutic effect of dihydroartemisinin (DHA) on tumor cells. However, the underlying mechanism of this has not yet been elucidated. The present study examined the potential therapeutic role and mechanism of DHA in T-cell lymphoma cells. It was revealed that DHA inhibited the proliferation of Jurkat and HuT-78 T-cell lymphoma cells in a concentration- and time-dependent manner. Furthermore, DHA reduced c-Myc protein expression at the transcriptional level, and induced the phosphorylation of c-Myc and the degradation of c-Myc oncoprotein levels. DHA treatment resulted in decreased phosphorylation of protein kinase B (Akt) and glycogen synthase 3β (GSK3β) in T-cell lymphoma cells. In addition, DHA treatment induced cell apoptosis, which was accompanied by an increased ratio of Bax/Bcl-2. Taken together, the results of the present study suggested that DHA may exert its antitumor role by accelerating c-Myc proteolysis and inhibiting the Akt/GSK3β pathway in T-cell lymphoma cells.
近期研究揭示了双氢青蒿素（DHA）对肿瘤细胞具有积极的治疗作用。然而，其潜在机制尚未阐明。本研究探讨了DHA在T细胞淋巴瘤细胞中的潜在治疗作用及机制。结果显示，DHA以浓度和时间依赖性方式抑制Jurkat和HuT-78 T细胞淋巴瘤细胞的增殖。此外，DHA在转录水平降低c-Myc蛋白表达，并诱导c-Myc磷酸化及c-Myc癌蛋白水平降解。DHA处理导致T细胞淋巴瘤细胞中蛋白激酶B（Akt）和糖原合酶3β（GSK3β）磷酸化水平降低。此外，DHA处理诱导细胞凋亡，同时伴有Bax/Bcl-2比值增加。综上所述，本研究结果提示，DHA可能通过加速c-Myc蛋白水解和抑制T细胞淋巴瘤细胞中的Akt/GSK3β途径发挥其抗肿瘤作用。
