Fenben, a anthelmintic drug used against parasites such as Ascaris and hookworm, also has demonstrated anti-cancer activity. It is thought to be an anti-neoplastic agent, destroying microtubules in cancer cells and causing them to collapse. It inhibits the growth of human xenografts in mice and boosts production of p53, a gene that can keep cancer cells in check. It has also been shown to block glucose uptake by cancer cells, down regulate expression of GLUT transporters and impair the enzymatic activity of hexokinase II (HK II) – a key glycolytic enzyme that most cancer cells thrive on.

Cellular responses to fenbendazole are complex and involve multiple mechanisms that lead to tumor regression, including the induction of autophagy and ferroptosis. In both 5-FU sensitive and resistant CRC cell lines, fenbendazole reduces tumorigenicity by either activating p53-mediated apoptosis or enhancing apoptosis through the mitochondrial p21 pathway. It also interferes with glucose uptake and alters cellular glycolysis by up-regulating the expression of autophagy proteins such as Beclin 1 and LC3-I.

The effect of fenbendazole on the survival of EMT6 tumors in a mouse model was evaluated using a colony formation assay with untreated and treated cultures grown in air and severe hypoxia. 2-h treatments with varying concentrations of fenbendazole induced a steep decrease in cell viability in the monolayer cultures, which reached a plateau when the drug concentration was increased to values approaching the limits of its solubility. Severe hypoxia significantly enhanced the toxicity of fenbendazole, but the number of surviving colonies in yield-corrected surviving fractions was not different from that in cultures treated under normal conditions. fenben cancer treatment

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