ArticleCell proliferation2007
Isothiocyanate E-4IB induces MAPK activation, delayed cell cycle transition and apoptosis.
Article in Cell proliferation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Pro-oncogenic and anti-oncogenic pathways: opportunities and challenges of cancer therapy.Future oncology (London, England) · 2010Review
- Silibinin suppresses growth of human prostate carcinoma PC-3 orthotopic xenograft via activation of extracellular signal-regulated kinase 1/2 and inhibition of signal transducers and activators of transcription signaling.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEpidemiologic studies point towards a significant correlation between the dietary intake of isothiocyanate-containing foods and the reduced risk for cancer. METHODS AND
resultsIn the current investigation, we examined the consequence of activating of signalling pathways during the release the cells from the block at G(1)/S boundary by synthetic isothiocyanate E-4IB. Using synchronized leukaemic HL60 cells, we show that activation of mitogen-activated protein kinases ERK1/2, c-Jun N-terminal kinase and p38 signalling pathways by E-4IB are coupled with delayed transition through the cell cycle and rapid cell cycle arrest resulted in diminished mitochondrial membrane potential culminating in apoptosis. These events were accompanied by histone deacetylase inhibition, increase of double strand DNA breaks detected by histone H2AX phosphorylation and up-regulation of cell cycle regulatory protein p21 and phosphorylation of CDC25C phosphatase.
conclusionThese findings suggest that the activation of mitogen-activated protein kinases signalling pathways, followed by the induction cell cycle arrest and apoptosis, might be responsible for anticancer activities of E-4IB.
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