Involvement of endoplasmic reticulum stress in Docetaxel-induced JNK-dependent apoptosis of human melanoma View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2008-11-07

AUTHORS

Nizar M. Mhaidat, Rick Thorne, Xu Dong Zhang, Peter Hersey

ABSTRACT

Our previous studies revealed that Docetaxel-induced apoptosis of melanoma cells is entirely dependent on activation of the JNK signalling pathway. Here, we show that Docetaxel-induced apoptosis is mediated by induction of ER stress. This was shown by Docetaxel-induced activation of proteins involved in ER stress signalling namely GRP78, ATF6, IRE1α, and PERK/eIF2α. Knockdown of IRE1α by siRNA markedly inhibited Docetaxel-induced JNK activation and downstream targets of JNK indicating that activation of IRE1α was upstream of activation of the JNK. Co-immunoprecipitation experiments showed that activation of JNK is due to activation of ASK1 through formation of an IRE1α-TRAF2-ASK1 complex. ER stress mediated activation of the JNK pathway is downstream of activation of PKCδ in that downregulation of PKCδ expression using specific PKCδ siRNA significantly inhibited Docetaxel-induced activation of IRE1α and the JNK pathway. These findings provide new insights to understand the mode of action of taxanes in treatment of human melanoma. More... »

PAGES

1505-1512

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10495-008-0276-8

DOI

http://dx.doi.org/10.1007/s10495-008-0276-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024056300

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18989785


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