Fenbendazole is an antiparasitic drug that has been shown to slow down cancer cell growth in petri dishes and mice. It is also able to block the formation of new tumors.
In our study, fenbendazole induced autophagy via Beclin-1 expression and apoptosis in both 5-FU-sensitive and -resistant colorectal cancer cells. It also inhibited glucose uptake and induced mitochondrial injury.
Inhibition of glucose uptake
Researchers have observed that fenbendazole blocks cancer cells’ ability to take in glucose, which is needed for their growth. This inhibition was due to a combination of mechanisms, including disruption of microtubules and activation of p53.
Microtubules are a protein scaffold that gives cells their shape and structure. Textbook depictions of cells often show them as floating bags of liquid, but they establish their shape through the cytoskeleton. This cellular structure is made of microtubules, which are also used to pull and separate the chromosomes during cell division. Drugs that interfere with the formation of microtubules stop important cellular processes, and this is how fenbendazole and other antiparasitic drugs kill parasites.
The researchers found that fenbendazole inhibits the growth of colorectal cancer cells in culture and also causes them to die in animals. They believe that this is because of its interference with glucose metabolism, which leads to apoptosis and other cell death pathways. They also noticed that fenbendazole triggered apoptosis in 5-fluorouracil-resistant SNU-C5/5-FUR cells without activating p53. This was due to decreased autophagy and reduced expression of SLC7A11 and GPX4.
While these findings are promising, there is no evidence that fenbendazole can cure cancer in humans. The drug has not been tested in clinical trials, and there is no guarantee that it will be safe for use as a treatment. A specialist cancer information nurse at Cancer Research UK told Full Fact that there is insufficient evidence that fenbendazole kills cancer cells, or that it prevents recurrent tumours.
Induction of apoptosis
The induction of apoptosis caused by fenbendazole has been shown to halt the growth of cancerous cells and inhibit their spread. It has also been shown to have minimal toxic effects on normal, healthy cells. This makes it a potential candidate for use in clinical trials, where it can be used to treat human cancers and other diseases.
The drug works by disrupting the formation of microtubules, a protein scaffold that helps establish the shape and structure of cells. It does this by binding to the cytoskeleton and blocking the synthesis of new microtubules. While textbook depictions of cells show them to float in amorphous bags of liquid, the fact is that they are established through the cytoskeleton, which comprises protein structures called microtubules.
These microtubules form a network of filaments that allow the cell to change shape and transport organelles and cargo around the body. But if cancer cells grow too large, these filaments can break, and the resulting damage can kill the cells. Fenbendazole prevents this by binding the cytoskeleton and blocking its formation.
Benzimidazoles, such as fenbendazole, are known to bind beta-tubulin and disrupt microtubules. They have been shown to bind mitochondrial DNA, induce necroptosis and apoptosis, and arrest cell cycle progression in colorectal cancer cells. Moreover, they have been shown to inhibit the RAS-related signaling pathway in lung cancer cells with a KRAS mutation.
Induction of cell cycle arrest
The benzimidazole carbamate fenbendazole is an antiparasitic drug that has also been shown to have anticancer properties. It binds to beta-tubulin and disrupts microtubules, causing cell cycle arrest and apoptosis. This effect is due to the interaction of fenbendazole with the mitochondrial GSH-GPX4 reductase complex. It also activates the p53-PARP signaling cascade and increases oxidative stress. In addition, fenbendazole triggers autophagy and ferroptosis in colorectal cancer cells.
The claim that fenbendazole cures cancer is based on anecdotal evidence from a single patient. This patient was a cancer survivor who claimed that he had cured his own small-cell lung cancer by taking fenbendazole. He told news outlets that he had taken the medication in conjunction with conventional cancer treatments. The claims were dismissed as unsubstantiated by other researchers.
In this study, researchers tested fenbendazole’s effects on a triple-negative breast cancer cell line (MDA-MB-231). The results showed that fenbendazole reduced the viability of the tumor cells by modulating their redox status. It increased the expression of GPX4, and suppressed the expression of SLC7A11, which resulted in ferroptosis and synergistic apoptosis. Treatment with the ferrostatin-1 and DFOM inhibitors failed to inhibit fenbendazole’s anti-cancer effects, suggesting that these mechanisms are the primary cause of fenbendazole’s cytotoxicity. In contrast, fenbendazole did not induce p53 activation in MDA-MB-231 cells. Moreover, its apoptosis effect was mediated through the mitochondrial injury and caspase-3-PARP signaling pathways.
Induction of DNA damage
In a recent study, researchers used fenbendazole (FZ) to inhibit glucose uptake in cancer cells and induce apoptosis. They found that the drug works by interfering with the formation of microtubules, a protein scaffolding that gives shape and structure to cells. Textbook depictions of cells often show various cellular organelles floating in amorphous bags of liquid, but cell structures actually establish their shape and physiology through the cytoskeleton, which is made up of a protein called tubulin. FZ interferes with the formation of this protein by blocking the binding of its components to each other.
The study also showed that fenbendazole can cause DNA damage in cancer cells and promote the formation of new mitochondria. This is because it inhibits the formation of a complex called cyclin D, which controls the entry of chromosomes into mitosis. The drug also interferes with the protein kinases p38, ERK, and JNK, which are involved in cell cycle control. Moreover, it activates p53 and blocks the entry of the cancerous gene c-Myc into mitosis.
Despite the fact that fenbendazole can suppress cancer growth in cell cultures and animal models, it hasn’t yet been shown to be effective as a cancer treatment in humans. There is no sufficient evidence that the drug can cure cancer, and it must be tested in randomized clinical trials to be proven safe and effective. fenbendazole for cancer