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Signal transduction activated by the cancer chemopreventive isothiocyanates: cleavage of BID protein, tyrosine phosphorylation and activation of JNK
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  • Published: 27 February 2001

Signal transduction activated by the cancer chemopreventive isothiocyanates: cleavage of BID protein, tyrosine phosphorylation and activation of JNK

  • K Xu1 &
  • P J Thornalley1 

British Journal of Cancer volume 84, pages 670–673 (2001)Cite this article

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Abstract

Phenethyl isothiocyanate and allyl isothiocyanate induce apoptosis of human leukaemia HL60 cells in vitro. Apoptosis was associated with cleavage of p22 BID protein to p15, p13 and p11 fragments and activation of JNK and tyrosine phosphorylation (18 kDa and 45 kDa proteins). All these effects and apoptosis were prevented by exogenous glutathione (15 mM). Protein tyrosine phosphatase activity was unchanged. The general caspase inhibitor Z-VAD-fmk prevented apoptosis but not JNK activation – excluding a role for caspases in JNK activation, whereas curcumin prevented JNK activation but only delayed apoptosis. This suggests that in isothiocyanate-induced apoptosis, the caspase pathway has an essential role, the JNK pathway a supporting role, and inhibition of protein tyrosine phosphatases is not involved. © 2001 Cancer Research Campaign

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  • 16 November 2011

    This paper was modified 12 months after initial publication to switch to Creative Commons licence terms, as noted at publication

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Authors and Affiliations

  1. Department of Biological Sciences, University of Essex, Central Campus, Wivenhoe Park, Colchester, CO4 3SQ, Essex, UK

    K Xu & P J Thornalley

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  1. K Xu
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  2. P J Thornalley
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From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

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Xu, K., Thornalley, P. Signal transduction activated by the cancer chemopreventive isothiocyanates: cleavage of BID protein, tyrosine phosphorylation and activation of JNK. Br J Cancer 84, 670–673 (2001). https://doi.org/10.1054/bjoc.2000.1636

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  • Received: 20 June 2000

  • Revised: 07 November 2000

  • Accepted: 17 November 2000

  • Published: 27 February 2001

  • Issue date: 02 March 2001

  • DOI: https://doi.org/10.1054/bjoc.2000.1636

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Keywords

  • isothiocyanate
  • BID
  • JNK
  • tyrosine phosphorylation
  • apoptosis

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  • Isothiocyanates: a class of bioactive metabolites with chemopreventive potential

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  • Mitochondrial translocation of cofilin is required for allyl isothiocyanate-mediated cell death via ROCK1/PTEN/PI3K signaling pathway

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