The role of inflammations and EMT in carcinogenesis

Abstract

Cancer is one of the major health burdens in modern world, and its mechanism is very complex, which is one of the main reasons for difficulties in cancer drug development. The development of cancer is associated with chronic inflammation, although inflammation is an essential biological process. The epithelial-mesenchymal transition (EMT) is a crucial step in development process of human tissue and involve in the regulatory pathways. On the contrary, the uncontrolled EMT is responsible for the initiation of cancer, its metastasis, immunosuppression, and resistance to antitumor treatment. Interestingly, there is an interrelationship between inflammation and EMT process. Usually, proinflammatory cytokines activate EMT inducing transcription factors (EMT-TFs), causing epithelial cells to change into cancerous mesenchymal cell by activating the mesenchymal cells markers, such as N- Cadherin, Fibronectin, Vimentin etc., and inhibiting the epithelial cells markers such as E− Cadherin, Claudin 1, Occludin, and β-catenin. Consequently, epithelial cells are dissociated, invasive, motile, resistant to therapy, resistant to apoptosis, and undergo mesenchymal cells angiogenesis. Some natural products and short RNAs have been identified to interfere with inflammation-EMT axis to inhibit cancer progression and metastasis. We have described these relationships in this review article and also described the therapeutic perspectives for cancer.