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Introduction
Mebendazole (MBZ), a drug traditionally used as an anthelmintic to treat parasitic worm infections, has shown potential as a cancer-fighting agent. This report compiles research findings on the efficacy of mebendazole in cancer prevention and treatment, its mechanisms of action, and its use in combination with other therapies.
Efficacy of Mebendazole in Cancer Prevention and Treatment
Research has demonstrated that mebendazole can significantly reduce tumor initiation and growth in preclinical models of colon cancer. A study combining mebendazole with the non-steroidal anti-inflammatory drug (NSAID) sulindac showed a 90% reduction in intestinal adenomas
. Mebendazole alone has also been effective in decreasing the number of intestinal adenomas by 56% , and has shown preclinical anti-cancer activity in various malignancies, including colorectal cancer . These findings support the potential for clinical trials in high-risk cancer patients
Mechanisms of Action
Mebendazole disrupts cancer cell function through several mechanisms. It interferes with tubulin formation, which is crucial for cell division
, and inhibits angiogenesis, the process by which tumors develop their own blood supply, by targeting VEGFR2 kinase activity . Mebendazole also induces apoptosis and suppresses oncogenes that drive cell proliferation and survival . Additionally, it has been found to impair tumor angiogenesis and reduce the expression of COX2 and various pro-inflammatory cytokines
Mebendazole in Hypoxic Cancer Environments
In breast cancer cells, mebendazole disrupts the activity of hypoxia-inducible factors (HIFs), which are proteins that help cancer cells survive in low-oxygen conditions
. By preventing the induction of HIF-1α, HIF-2α, and HIF-1β proteins under hypoxia, mebendazole may have additional therapeutic efficacy in these challenging environments
Mebendazole and Radiotherapy
Mebendazole has been shown to enhance the anticancer activity of radiotherapy (RT) in radiotherapy-resistant triple-negative breast cancer (TNBC) cells. It increases the effectiveness of RT in terms of reducing cell viability and colony formation
, and when combined with RT, it more effectively reduces cell migration and invasion . The combination therapy also enhances the expression of Cyclin B1 and pH2AX levels, which are markers of DNA damage and cell cycle arrest . Importantly, mebendazole enhances natural killer (NK) cell-mediated cytotoxicity in RT treatment, which is a critical component of the immune system's ability to target and destroy cancer cells
Conclusion
Mebendazole has emerged as a promising candidate for cancer treatment, with a range of mechanisms that disrupt cancer cell growth and survival. Its ability to work synergistically with other treatments, such as NSAIDs and radiotherapy, further enhances its potential as a therapeutic agent. The low toxicity profile of mebendazole and its preclinical success in various cancer models warrant further investigation and consideration for clinical trials in cancer patients.
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