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Targeting nuclear factor-kappa B to overcome resistance to chemotherapy.
Intrinsic or acquired resistance to chemotherapeutic agents is a common phenomenon and a major challenge in the treatment of cancer patients. Chemoresistance is defined by a complex network of factors including multi-drug resistance proteins, reduced cellular uptake of the drug, enhanced DNA repair, intracellular drug inactivation, and evasion of apoptosis. Pre-clinical models have demonstrated that many chemotherapy drugs, such as platinum-based agents, antracyclines, and taxanes, promote the activation of the NF-?B pathway. NF-?B is a key transcription factor, playing a role in the development and progression of cancer and chemoresistance through the activation of a multitude of mediators including anti-apoptotic genes. Consequently, NF-?B has emerged as a promising anti-cancer target. Here, we describe the role of NF-?B in cancer and in the development of resistance, particularly cisplatin. Additionally, the potential benefits and disadvantages of targeting NF-?B signaling by pharmacological intervention will be addressed.
Keyword(s): oncogene; apoptosis; resistance; chemotherapy; cisplatin; cancer; NF-?B; Cancer; Biomedical sciences
Publication Date:
Type: Journal article
Peer-Reviewed: Yes
Language(s): English
Institution: Trinity College Dublin
Citation(s): Godwin P, Baird AM, Heavey S, Barr MP, O'Byrne KJ, Gately K., Targeting nuclear factor-kappa B to overcome resistance to chemotherapy., Frontiers in oncology, 3, 2013, 120
First Indexed: 2014-09-09 05:43:45 Last Updated: 2019-11-29 06:46:11