Abstract | BACKGROUND: METHODS: We generated drug-resistant cells by continuous exposure to chemotherapeutic drugs and analyzed the mechanism(s) of therapy resistance in malignant melanoma. RESULTS: We report chemotherapies induced upregulation of a variety of chemokines in the CXCR1/CXCR2 network by an NF-κB-dependent mechanism. Notably, analysis of the drug-resistant melanoma cell line selected after prolonged exposure to chemotherapeutic drug dacarbazine revealed higher levels of CXCL8 and CXCR2 compared with parent cells as a signature of drug resistance. CXCR2 neutralization markedly improved sensitivity to dacarbazine in melanoma cells. CONCLUSION:
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Authors | S Wu, S Saxena, M L Varney, R K Singh |
Journal | Current molecular medicine
(Curr Mol Med)
Vol. 17
Issue 6
Pg. 436-449
( 2017)
ISSN: 1875-5666 [Electronic] Netherlands |
PMID | 29256349
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Copyright | Copyright© Bentham Science Publishers; For any queries, please email at [email protected]. |
Chemical References |
- Antineoplastic Agents, Alkylating
- CXCR2 protein, human
- NF-kappa B
- Receptors, Interleukin-8A
- Receptors, Interleukin-8B
- Dacarbazine
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Topics |
- Antineoplastic Agents, Alkylating
(pharmacology)
- Dacarbazine
(pharmacology)
- Drug Resistance, Neoplasm
- Gene Expression Regulation, Neoplastic
(drug effects)
- Humans
- Melanoma
(drug therapy, metabolism, pathology)
- NF-kappa B
(genetics, metabolism)
- Receptors, Interleukin-8A
(genetics, metabolism)
- Receptors, Interleukin-8B
(genetics, metabolism)
- Signal Transduction
- Tumor Cells, Cultured
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