MAPK signaling in inflammation-associated cancer development

Abstract

Mitogen-activated protein (MAP) kinases comprise a family of protein-serine/threonine kinases, which are highly conserved in protein structures from unicellular eukaryotic organisms to multicellular organisms, including mammals. These kinases, including ERKs, JNKs and p38s, are regulated by a phosphorelay cascade, with a prototype of three protein kinases that sequentially phosphorylate one another. MAPKs transduce extracellular signals into a variety of cellular processes, such as cell proliferation, survival, death, and differentiation. Consistent with their essential cellular functions, MAPKs have been shown to play critical roles in embryonic development, adult tissue homeostasis and various pathologies. In this review, we discuss recent findings that reveal the profound impact of these pathways on chronic inflammation and, particularly, inflammation-associated cancer development.

Lactobacillus plantarum Lipoteichoic Acid Alleviates TNF-α-Induced Inflammation in the HT-29 Intestinal Epithelial Cell Line

“…The transcription factors NF-κB and MAPKs are particularly important in colon cancer development (Danese and Mantovani, 2010;Huang et al, 2010). Activation of NF-κB contributes to the activation of innate immunity, inflammation, cell proliferation, and survival.…”

Lactotransferrin expression is downregulated and affects the mitogen-activated protein kinase pathway in gastric cancer

“…The results demonstrated that overexpression of LTF downregulated the expression of p38, JNK2 and c-Jun in the SGC7901 cells. MAPKs transduce extracellular signals, promoting a variety of cellular processes, including cell proliferation, survival, death and differentiation (29). JNK and p38 MAPK signaling are associated with various types of cancer in humans and mice (30).…”

Pathophysiological significance and therapeutic targeting of germinal center kinase in diffuse large B-cell lymphoma

“…16,28,29 Prior to this study, aberrations in MAPK signaling have been linked to a variety of cancers but not to the pathogenesis of DLBCL tumors. 16,[30][31][32] Our specific findings include previously unknown activation of the GCK signaling pathway in DLBCL. We further demonstrate that GCK knockdown in DLBCL leads to decreased proliferation and cell death.…”