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- W2052661138 abstract "Cancer is a group of diseases characterized by uncontrolled cell proliferation, evasion of cell death and the ability to invade and disrupt vital tissue function. The classic model of carcinogenesis describes successive clonal expansion driven by the accumulation of mutations that eliminate restraints on proliferation and cell survival. It has been proposed that during cancer's development, the loose-knit colonies of only partially differentiated cells display some unicellular/prokaryotic behavior reminiscent of robust ancient life forms. The seeming “regression” of cancer cells involves changes within metabolic machinery and survival strategies. This atavist change in physiology enables cancer cells to behave as selfish “neo-endo-parasites” that exploit the tumor stromal cells in order to extract nutrients from the surrounding microenvironment. In this framework, it is conceivable that anti-parasitic compounds might serve as promising anticancer drugs. Nitazoxanide (NTZ), a thiazolide compound, has shown antimicrobial properties against anaerobic bacteria, as well as against helminths and protozoa. NTZ has also been successfully used to promote Hepatitis C virus (HCV) elimination by improving interferon signaling and promoting autophagy. More compelling however are the potential anti-cancer properties that have been observed. NTZ seems to be able to interfere with crucial metabolic and pro-death signaling such as drug detoxification, unfolded protein response (UPR), autophagy, anti-cytokine activities and c-Myc inhibition. In this article, we review the ability of NTZ to interfere with integrated survival mechanisms of cancer cells and propose that this compound might be a potent addition to the current chemotherapeutic strategy against cancer." @default.
- W2052661138 created "2016-06-24" @default.
- W2052661138 creator A5043951441 @default.
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- W2052661138 date "2014-10-01" @default.
- W2052661138 modified "2023-10-06" @default.
- W2052661138 title "A functional perspective of nitazoxanide as a potential anticancer drug" @default.
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- W2052661138 doi "https://doi.org/10.1016/j.mrfmmm.2014.05.005" @default.
- W2052661138 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25847384" @default.
- W2052661138 hasPublicationYear "2014" @default.
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