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-κB pathway. NF-κB 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-κB has emerged as a promising anti-cancer target. Here, we describe the role of NF-κB in cancer and in the development of resistance, particularly cisplatin. Additionally, the potential benefits and disadvantages of targeting NF-κB signaling by pharmacological intervention will be addressed.
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|Keywords:||Apoptosis, Cancer, Chemotherapy, Cisplatin, NF-κB, Oncogene, Resistance, 4 (2 aminoethylamino) 1, 8 dimethylimidazo [1, 2 a] quinoxaline, 4 (2 aminoethylamino) 1, 8 dimethylimidazo[1, 2 a]quinoxaline, bindarit, bioperine, black pepper extract, bortezomib, carboplatin, caspase 8, CD40 antigen, curcumin, cyclin D, cyclin dependent kinase 2, cycloheximide, cyclooxygenase 2 inhibitor, docetaxel, Fas antigen, FLICE inhibitory protein, immunoglobulin enhancer binding protein, paclitaxel, parthenolide, phosphatidylethanolamine binding protein, polo like kinase 3, protein p100, protein p53, stress activated protein kinase, synaptotagmin I, temozolomide, tumor necrosis factor receptor, tumor necrosis factor related apoptosis inducing ligand, unclassified drug, unindexed drug, cancer chemotherapy, cell proliferation, DNA damage, gene mutation, genetic transcription, head and neck cancer, human, lung non small cell cancer, neoplasm, nonhuman, ovary cancer, pancreas cancer, phase 2 clinical trial (topic), promoter region, protein degradation, protein expression, protein phosphorylation, review, signal transduction, solid tumor|
|Subjects:||Australian and New Zealand Standard Research Classification > MEDICAL AND HEALTH SCIENCES (110000) > ONCOLOGY AND CARCINOGENESIS (111200)|
|Divisions:||Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
|Copyright Owner:||Copyright 2013 The Author(s)|
|Deposited On:||26 Feb 2014 00:36|
|Last Modified:||30 Jul 2014 22:47|
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