The deworming medication fenben, which is sold in Canada as a veterinary product, has been hailed as a cancer cure by some online users who say that it has eradicated their disease. The antiparasitic drug is used to treat parasitic infections in cattle and sheep. It has also been shown to reduce the spread of bovine respiratory tract infections and aid in milk production. However, Health Canada lists fenben as a veterinary drug for anthelmintic treatment only and has not approved it for use in humans. McMaster University researcher Sheila Singh says there is no evidence to support claims that fenben can cure human cancer.
Singh’s team has analyzed tumour samples from the cancer patients who made such claims and found that these patients had normal genetic and molecular makeup, with no signs of preexisting tumours or mutations in their DNA. In fact, they had a very low risk of cancer to begin with, and most of the tumours were of very small size. Singh’s research was prompted by a series of videos posted in 2023 on Facebook and TikTok, where a veterinarian claimed that fenben could cure cancer in humans. The vet was subsequently banned from practicing in the province of British Columbia after the College of Veterinarians received complaints about his content.
Our data suggest that fenben causes changes in the organisation of the microtubule network in cancer cells. This change is caused by a direct binding of the drug to tubulin, resulting in distorted polymerization and depolymerization, as shown in Figure 2b. This is in contrast to colchicine treatment, which has no effect on the structure of the microtubule network and leads to complete depolymerization of microtubules.
The ability of fenben to alter the microtubule structure was further confirmed by our experiments in which tubulin was incubated with DMSO or FZ, and the effects on polymerization were monitored spectrophotometrically. The presence of the drug led to a decrease in polymerization, as measured by a reduction in turbidity at 340 nm (Fig. 2c). FZ also did not interact with the P-gp protein and inhibit its function, as assessed by a competition assay in which the P-gp substrate verapamil was added.
We next studied the effect of fenbendazole on the growth of EMT6 tumors in mice, using a rigorous colony formation assay. 24-h incubation with fenbendazole reduced both the clonogenicity and cell numbers of the tumours, indicating that it has cytotoxic as well as cytostatic properties.
Finally, we tested whether the fenbendazole-induced alterations in the microtubule network affected cell cycle progression by treating synchronized A549 cells with different concentrations of FZ and measuring mitosis-promoting complex (MPC) activity by comparing the accumulation of the red MPC marker rhodamine 123 to that of untreated control cells. Our results showed that increasing concentrations of fenbendazole led to enhanced translocation of WT p53 from the cytoplasm to mitochondria, accompanied by increased MPC activity. These results are consistent with the hypothesis that a mild disruption of the microtubule network by fenbendazole is sufficient to activate p53, which is then capable of enhancing cell death.