2. Academic Validation
  3. Flubendazole inhibits glioma proliferation by G2/M cell cycle arrest and pro-apoptosis

Flubendazole inhibits glioma proliferation by G2/M cell cycle arrest and pro-apoptosis

  • Cell Death Discov. 2018 Feb 14;4:18. doi: 10.1038/s41420-017-0017-2.
Xumin Zhou 1,  Jumei Liu 1,  Jinming Zhang 2,  Yong Wei 1,  Hua Li 1
Affiliations

Affiliations

  • 1 1Department of Pathogen Biology and Experimental teaching center of Preventive Medicine, Guangdong Provincial Key Laboratory of Tropical Disease, School of Public Health, Southern Medical University, Guangzhou, 510515 China.
  • 2 2Department of Respiration, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 China.
PMID: 29531815 DOI: 10.1038/s41420-017-0017-2
Abstract

Flubendazole, FDA-approved anthelmintic, has been widely used in treating testinal parasites. In the recent years, Flubendazole has been reported to exert Anticancer activities. On the other hand, little was known about the effects of Flubendazole on gliomas. Here we demonstrated a novel effect of flubendazole on glioma cells. We found that Flubendazole inhibited cell proliferation and promoted cell Apoptosis of glioma cell lines in vitro, and suppressed tumor growth in xenograft models by intraperitoneal injection. However, Flubendazole might have no influence on cell migration. Mechanism study reaveled that Flubendazole caused cell cycle arrest in G2/M phase, which partly account for the suppressed proliferation. Consistently, Flubendazole induced P53 expression and reduced Cyclin B1 and p-cdc2 expression in glioma cells. In addition, Flubendazole promoted cell Apoptosis by regulating the classical Apoptosis protein Bcl-2 expression. These observations suggest that Flubendazole exerts anti-proliferation and pro-apoptosis effects in Glioma through affecting the cell cycle and intrinsic apoptotic signaling, and indicate a novel utilization of Flubendazole in the treatment of Glioma.

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