Research progress on mechanism of inflammatory signaling pathway-driven cancer induced by arsenide
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Abstract
Cancer has become one of the most serious diseases which severely harm the health of human beings and the development of human society, and it has been a serious public health problem that the world has to face. Studies show that 20% cancers are related closely with chronic inflammation, and more and more scholars pay attention to the mechanism of environmental carcinogen on tumorigenesis through inflammatory reaction. Arsenide as an environmental carcinogen can generate both acute and chronic toxicity, induce the overexpression of inflammatory cytokines, change cellular microenvironment, and result in tumorigenesis. Interestingly, Chinese traditional arsenic medicine can inhibit tumor growth through regulating inflammatory signaling pathways, and have a good application prospect in tumor therapy, such as leukemia treatment. Therefore, arsenide has two totally different biological effects, carcinogenic and anticarcinogenic. Research indicates that arsenide can regulate the number and activity of transcript factors such as nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1), influence the expressions of inflammatory cytokines such as cyclooxygenase-2 (COX-2) and tumor necrosis factor-α (TNF-α), lead to changes in bioactivity like cell apoptosis and adhesion, and then regulate tumorigenesis development. In order to further illustrate the molecular mechanism of how arsenide regulates tumorigenesis through different inflammatory signaling pathways, the review summarized evidence linking inflammatory microenvironment to tumor growth and shrinkage regulated by arsenide.
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