सेल संकेतन जर्नल
खुला एक्सेस
आईएसएसएन: 2576-1471
आईएसएसएन: 2576-1471
Xiaomei Hou, Fan Yang, Wenbin Liu, Zhongxing Fu, Lei Chen, Zixiong Li, Chong Ni, Min Liu and Guangwen Cao*
Recently, growing evidences have shown that chronic inflammation is the major cause of carcinogenesis. Inflammation signaling pathways can facilitate evolution and development of cancers in a variety of aspects, such as proliferation, metastasis, and apoptosis, etc. Nuclear factor-kappa B (NF-κB), janus-activated kinase (JAK)-signal transducers and activators 3 (STAT3), mitogen-activated protein kinase (MAPK), phosphatidylinositol-3-kinase/ protein kinase B (PKB, also known as Akt)/ mammalian target of rapamycin (PI3K/Akt/mTOR), Wnt/ β-catenin, and transforming growth factor (TGF)-β/Smad signaling pathways have been well studied, which are implicated in inflammation-induced carcinogenesis. Although tremendous of researches have reported these signaling pathways, few has explained the mechanism by which inflammation signaling pathways sustain activation during carcinogenesis. In this review, we summarized the present knowledge of 6 well known inflammation signaling pathways, especially their roles in chronic inflammation-induced carcinogenesis, reasons for the persistent inflammation, and potential inhibitors targeting key molecules for cancer therapy. This review will help in improving our understandings of how these inflammation signaling pathways take part in carcinogenesis, thus paving the way for the prediction of occurrence and prognosis as well as targeting therapy of cancers.