Inflammation, cancer and chemoresistance: taking advantage of the toll-like receptor signaling pathway.
The association between chronic inflammation and cancer has long been observed. Furthermore, NF-kappaB activation and the subsequent production of cytokines, chemokines, growth factors, and antiapoptotic proteins has been found to be involved in cancer progression and chemoresistance. However, the signals inducing NF-kappaB in cancer cells are still not well understood. Here, we reviewed the association between chronic inflammation and cancer, the role of NF-kappaB and its inhibitors as potential anticancer drugs, and Toll-like receptors as possible signal initiators for NF-kappaB activation and inflammation-induced carcinogenesis and chemoresistance. Furthermore, we propose that, the stimulation of Toll-like receptors by microbial components and/or endogenous ligands may represent the initial signal promoting a proinflammatory environment that will enhance tumor growth and chemoresistance.
Chen
Rui
R
Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520, USA.
Alvero
Ayesha B
AB
Silasi
Dan-Arin
DA
Mor
Gil
G
D000818:Animals; D019008:Drug Resistance, Neoplasm; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology; D053594:Myeloid Differentiation Factor 88 / Q000276:immunology / Q000378:metabolism; D016328:NF-kappa B / Q000276:immunology / Q000494:pharmacology; D009369:Neoplasms / Q000188:drug therapy* / Q000276:immunology* / Q000378:metabolism; D010051:Ovarian Neoplasms / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors / Q000276:immunology* / Q000378:metabolism
D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors