Fenbendazole For Cancer Induces P53-Induced Apoptosis

Fenben is a benzimidazole drug used to treat parasitic infections including pinworms, giardia, roundworms, hookworms, Taenia solium, and pulmonary paragonimiasis. It has also been proposed that fenben may be useful in fighting cancer, especially non-small cell lung cancer (NSCLC), as it has been shown to reactivate p53 and induce apoptosis in cancer cells. However, the p53-induced apoptosis induced by fenben for cancer is controversial as it is accompanied by severe liver damage in some patients. In addition, it is important to note that fenben does not reactivate p53 in all cancers and does not protect against cellular mutations or suppress tumor progression.

The proliferation of cancer cells requires energy and is accelerated by glycolysis, the oxidative degradation of glucose to acetyl-CoA. The benzimidazole compounds interfere with host energy metabolism and inhibit glucose uptake. This mechanism of action is responsible for the antiparasitic and anthelmintic effects of the drugs. The p53-dependent apoptosis induced by the benzimidazoles is due to the disruption of microtubule dynamics and modulation of genes involved in multiple cellular pathways.

It has been known for a long time that malignant cells exhibit distinct metabolic profiles compared with normal cell lines. In particular, cancer cells consume glucose several folds more than the normal cells. The glucose uptake into the cell is controlled by GLUT transporters and key glycolytic enzymes. Glucose deprivation is a promising strategy for enhancing the efficacy of chemotherapeutic agents. Several benzimidazoles have been found to inhibit glucose uptake in cancer cells and thus to induce apoptosis. Among them, fenbendazole is one of the most potent.

In our study, fenbendazole for cancer significantly decreased glucose uptake into H460 and A549 NSCLC cells. This effect was mediated by the inhibition of GLUT transporters and the enzymatic activity of HKII. Moreover, fenbendazole induced apoptosis and inhibited the cell cycle in both 5-FU-sensitive SNU-C5 and SNU-C5/5-FUR colorectal cancer cells. The apoptosis was associated with activation of p53, autophagy, and ferroptosis.

The acquisition and perception of false information by patients triggered by the fenben for cancer scandal have been discussed. To investigate this issue, we conducted semi-structured interviews with cancer patients. Our results showed that the patients acquired information about fenben from social media channels, and most were aware of Joe Tippens’ YouTube video as the source of this information. In addition, many of the patients actively cross-checked information and sought out reliable sources to confirm the facts. Nevertheless, the information they obtained was fragmented and incomplete as it was processed through various media channels. This resulted in a misinterpretation of the information, which led to a serious adverse reaction to fenben. In order to prevent such a situation, health authorities should actively promote communication with patients. They should present empirical evidence and support patients to make informed decisions about alternative medicine. Moreover, they should provide appropriate education to help cancer patients evaluate the information on the Internet. The underlying cause of this problem is the lack of clear information from the media on the risks and benefits of complementary alternative medicine.

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