Recently, posts claiming that fenben (a deworming medicine) cures cancer in humans have gained traction on social media. Health Feedback explains why this claim is false. We interviewed lung cancer patients about their acquisition channels of complementary and alternative medicine information, the quality of the obtained information, and their perceptions on the effectiveness of fenben for their cancer treatment. Anti-cancer activity Benzimidazole anthelmintic agents have been repurposed for cancer therapy because of their ability to inhibit cell growth. However, there is no direct evidence that these compounds have anti-cancer activity in humans. In this study, the authors examined the effect of fenbendazole on glucose uptake in H460 and A549 human cancer cells. They found that fenbendazole (FZ) caused a significant reduction in glucose uptake and metabolite formation by these cells. They also performed a glucose uptake assay with the fluorescent glucose analogue 2-NBDG, which revealed that FZ induced inhibition in glycolysis and gluconeogenesis. Rather than floating in amorphous bags of liquid, as depicted in textbooks, cells establish shape and structure through a protein scaffolding called the cytoskeleton. The cytoskeleton is composed of microtubules, which are derived from a protein called tubulin. Because of its ability to depolymerize microtubules, fenbendazole can inhibit cancer cell growth and promote cell death through multiple pathways. However, a randomized clinical trial would be needed to confirm this claim. Anti-proliferative activity Fenbendazole is an antiparasitic drug that interferes with microtubule formation, a protein scaffolding within cells. It also blocks cell division and induces apoptosis in cancer cells. These properties make it a promising candidate as an alternative or supplementary cancer therapy. Textbook depictions of cells show cellular components floating in amorphous bags of liquid, but this is far from the truth. Cells establish shape and structure through a complex scaffolding called the cytoskeleton, which is composed of a protein called tubulin. These proteins are able to assemble and disassemble as needed, such as when a cell changes shape to move through narrow spaces or divides to produce two identical cells. Treatment of wild-type and 5-fluorouracil-resistant SNU-C5 colorectal cancer cells with fenbendazole (FZ) resulted in reduced viability. A glucose uptake assay was performed, and the results indicated that FZ inhibited glycolysis. Additionally, a flow cytometry assay revealed that FZ induced ferroptosis and cell cycle arrest in both cell types. Apoptosis Fenbendazole (FZ), a cheap anti-parasitic medication used as dog dewormer, has been shown to boost the production of cancer-killing enzymes. It also destroys microtubules that sustain cancer cell growth. Its anecdotal success stories have led to its repurposing as a cancer treatment, especially in combination with other drugs. Benzimidazole agents are known to enhance the cytotoxicity of chemotherapeutic agents and reduce multidrug resistance in resistant cancers. However, few studies have evaluated the underlying mechanisms of benzimidazole in resistant cancers. In this study, we determined the apoptosis activity of FZ in 5-fluorouracil-resistant SNU-C5 colorectal cancer cells and compared it with that of albendazole. We found that FZ suppressed the proliferation of resistant colorectal cancer cells via G2/M arrest and ferroptosis-augmented apoptosis. It also enhanced the cytotoxicity of radiation and doxorubicin in a p53-dependent manner. In addition, FZ increased integrin aV and n-cadherin expression and inhibited glycolytic changes and the generation of ROS in resistant cells. A clonogenic assay revealed that both free FEN and the FEN/RAPA-loaded mPEG-b-PCL micelle equally inhibited colony formation at 2090 nM and induced apoptosis in both cell groups. Necroptosis Scientists at NCI have found that injecting cells undergoing a type of cell death called necroptosis can prompt the immune system to eliminate cancer tumors in mice. The team used a virus to deliver genes for the protein kinase RIPK3 into tumor cells, which activates necroptosis. The dead cancer cells then swell and burst, producing chemicals that change the tumor microenvironment to recruit and activate phagocytes—a type of immune cell that engulfs and destroys unwanted cells. The scientists also fed the fenbendazole diet to mice with human lymphoma xenografts, and found that the drug prevents them from growing. This effect could be due to its disruption of glycolysis, a process that fuels cancer growth and is known as the Warburg effect. A similar effect has been observed in mice treated with a pinworm medication, Aspiculuris tetraptera, to disrupt glycolysis. However, the researchers aren’t sure how these two drugs act synergistically to inhibit tumor growth. Their study is published in the journal Science Immunology. fenben for cancer
Is Fenben For Cancer True?
