TY - JOUR
T1 - Mebendazole is a potent inhibitor to chemoresistant T cell acute lymphoblastic leukemia cells
AU - Wang, Xiaolei
AU - Lou, Kaiyan
AU - Song, Xiaodong
AU - Ma, Huijuan
AU - Zhou, Xinyi
AU - Xu, Huan
AU - Wang, Wei
N1 - Funding Information:
This work was funded by National Natural Science Foundation of China [grant No. 21906057 to H.X., grant No. 21738002 to W.W., grant No. 21577037 to K.L.] and Shanghai Science and Technology Committee through the Shanghai Sailing Program [grant No. 19YF1412500 to H.X.].
Publisher Copyright:
© 2020 Elsevier Inc.
PY - 2020/6/1
Y1 - 2020/6/1
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Chemoresistance
KW - Drug repurposing
KW - Mebendazole
KW - Notch1
KW - T cell acute lymphoblastic leukemia
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U2 - 10.1016/j.taap.2020.115001
DO - 10.1016/j.taap.2020.115001
M3 - Article
C2 - 32277947
AN - SCOPUS:85082879967
VL - 396
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
SN - 0041-008X
M1 - 115001
ER -