• Chemokines;
  • chemoresistance;
  • epithelial ovarian cancer;
  • MyD88;
  • paclitaxel;
  • Toll-like receptor

The association between chronic inflammation and cancer has long been observed. Furthermore, NF-κB 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-κB in cancer cells are still not well understood. Here, we reviewed the association between chronic inflammation and cancer, the role of NF-κB and its inhibitors as potential anticancer drugs, and Toll-like receptors as possible signal initiators for NF-κB 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.