Abstract
Flubendazole, belonging to benzimidazole, is a broad-spectrum insect repellent and has been repurposed as a promising anticancer drug. In recent years, many studies have shown that flubendazole plays an anti-tumor role in different types of cancers, including breast cancer, melanoma, prostate cancer, colorectal cancer, and lung cancer. Although the anti-tumor mechanism of flubendazole has been studied, it has not been fully understood. In this review, we summarized the recent studies regarding the anti-tumor effects of flubendazole in different types of cancers and analyzed the related mechanisms, in order to provide the theoretical reference for further studies in the future.
Highlights
Flubendazole(FLU)([5-(4-fluorobenzoyl)-1H-benzimidazole-2-y1]-carbamic acid methyl ester) (Figure 1), which was developed by Janssen in the 1970s, belongs to the group of benzimidazole anthelmintics and is widely used in the treatment of helminth and intestinal parasite infection [1,2,3,4,5]
The anthelmintic effect of FLU is based on its ability to change microtubule structure, inhibit tubulin polymerization, destroy microtubule function, and interfere with the transport of secretory vesicles mediated by the microtubule in the absorptive tissues of helminths [4,8,9,10,11]
It has been reported that FLU plays an important anti-tumor role in many kinds of cancers, such as breast cancer, melanoma, neuroblastoma, colorectal cancer, liver cancer, oral squamous cell cancer [1,10,14,15,16,17,18,19,20,21,22,23,24], and is regarded as a promising anti-tumor drug [1,22]
Summary
Flubendazole(FLU)([5-(4-fluorobenzoyl)-1H-benzimidazole-2-y1]-carbamic acid methyl ester) (Figure 1), which was developed by Janssen in the 1970s, belongs to the group of benzimidazole anthelmintics and is widely used in the treatment of helminth and intestinal parasite infection [1,2,3,4,5]. Recent studies have shown that FLU inhibits cell proliferation and delays tumor formation in xenograft models and shows preclinical activity by suppressing tubulin polymerization in lymphoma and leukemia [10,25,26]. The results of Zhi-Jie Hou et al showed that FLU suppressed the proliferation of breast cancer which enriched CS-like cells in a dose- and time-dependent manner and reduced the tumor volume of the xenograft model by intraperitoneal injection. FLU suppressed the cell migration and reversed the epithelial-mesenchymal transition (EMT) phenotype by decreasing the expression of mesenchymal markers (β-catenin, N-cadherin, and Vimentin) and promoting the expression of the epithelial and differentiation marker (Keratin 18) in CS-like cells-enriched breast cancer, indicating that FLU inhibited breast cancer metastasis. The further study showed that FLU inhibited cell cycle at the G2/M phase and promoted the monopolar spindle formation by suppressing tubulin polymerization in breast cancer cells, which inhibited CS-like cells capability. FLU could ameliorate breast cancer through inhibiting proliferation, metastasis, and drug resistance mainly by inhibiting breast CS-like cells in CS-like cells-enriched breast cancer via inhibiting cell cycle progression and tubulin polymerization [24]
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