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.
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