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. 2011 Jan 18;104(3):437–440. doi: 10.1038/sj.bjc.6606065

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Copyright © 2011 Cancer Research UK

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Suggested pathway illustrating the influence of monoHER on doxorubicin cytotoxicity in WLS-160 cells. Under resting conditions, NF-κB is maintained in an inactive state in the cytoplasm via interaction with the inhibitory protein, IκB. Doxorubicin can activate the NF-κB pathway, which involves the phosphorylation, ubiquitination and proteasomal degradation of IκB. Nuclear factor-κB is then free to translocate to the nucleus where it facilitates the transcription of, for example, antiapoptotic genes, resulting in less tumour cell killing and the development of drug resistance. MonoHER is able to reduce this doxorubicin-induced NF-κB activation, thereby sensitising WLS-160 cells to doxorubicin-induced apoptosis.