Mebendazole is a potent inhibitor to chemoresistant T cell acute lymphoblastic leukemia cells

被引:15
|
作者
Wang, Xiaolei [1 ,2 ]
Lou, Kaiyan [1 ,2 ]
Song, Xiaodong [3 ]
Ma, Huijuan [1 ,2 ]
Zhou, Xinyi [1 ,2 ]
Xu, Huan [1 ,2 ]
Wang, Wei [1 ,2 ,4 ,5 ]
机构
[1] East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
[2] East China Univ Sci & Technol, Sch Pharm, Dept Pharmaceut Sci, Shanghai 200237, Peoples R China
[3] Fudan Univ, Hua Shan Hosp North, Med Lab Dept, Shanghai 201907, Peoples R China
[4] Univ Arizona, Dept Pharmacol & Toxicol, Tucson, AZ 85721 USA
[5] Univ Arizona, BIO5 Inst, Tucson, AZ 85721 USA
基金
中国国家自然科学基金;
关键词
Mebendazole; T cell acute lymphoblastic leukemia; Notch1; Drug repurposing; Apoptosis; Chemoresistance; C-MYC; TRANSPORTERS; RESISTANCE; APOPTOSIS; NOTCH1; MECHANISMS; THERAPIES; EFFICACY; GROWTH; MICE;
D O I
10.1016/j.taap.2020.115001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Mebendazole (MBZ) is a tubulin-suppressive antihelmintic agent with low toxicity, which has been repurposed to treat different types of tumors. Chemoresistance is quite common in refractory or relapsed T cell acute lymphoblastic leukemia (T-ALL), which leads to dismal chances of recovery. In this study, MBZ was found to suppress the proliferation and reduce the viability of T-ALL cell line, CCRF-CEM, and its chemoresistant derivative, CEM/C1, at nanomolar concentrations. The inhibitive effects were found to be dose-dependent and not to be affected by the chemoresistance of CEM/C1 cells. Cell cycle arrest, caspase 3/7 activation and tubulin disruption were found in the MBZ-treated T-ALL cells. Notch1 signaling, which is often aberrantly activated in T-ALL cells, was showed to be suppressed by MBZ treatments. MBZ administration in murine T-ALL models also suppressed the growth of CEM/C1 cells, indicating that MBZ may be developed as a therapeutic agent for chemoresistant T-ALLs. The mRNA levels of the Notch1 and Hes1 were also confirmed to be suppressed by MBZ in vivo, which was consistent with the in vitro observations. This study demonstrated, for the first time, that MBZ could inhibit chemoresistant T-ALL cells both in vitro and in vivo, and the Notch1 signaling pathway was suppressed by MBZ treatment.
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页数:9
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