ArticleJournal of carcinogenesis2007
Persistent activation of NF-kappaB related to IkappaB's degradation profiles during early chemical hepatocarcinogenesis.
Article in Journal of carcinogenesis, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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0 citing papers in PubMed, 7 citations in OpenAlex.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
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Abstract
backgroundTo define the NF-kappaB activation in early stages of hepatocarcinogenesis and its IkappaB's degradation profiles in comparison to sole liver regeneration.
methodsWestern-blot and EMSA analyses were performed for the NF-kappaB activation. The transcriptional activity of NF-kappaB was determined by RT-PCR of the IkappaB-alpha mRNA. The IkappaB's degradation proteins were determined by Western-blot assay.
resultsWe demonstrated the persistent activation of NF-kappaB during early stages of hepatocarcinogenesis, which reached maximal level 30 min after partial hepatectomy. The DNA binding and transcriptional activity of NF-kappaB, were sustained during early steps of hepatocarcinogenesis in comparison to only partial hepatectomy, which displayed a transitory NF-kappaB activation. In early stages of hepatocarcinogenesis, the IkappaB-alpha degradation turned out to be acute and transitory, but the low levels of IkappaB-beta persisted even 15 days after partial hepatectomy. Interestingly, IkappaB-beta degradation is not induced after sole partial hepatectomy.
conclusionWe propose that during liver regeneration, the transitory stimulation of the transcription factor response, assures blockade of NF-kappaB until recovery of the total mass of the liver and the persistent NF-kappaB activation in early hepatocarcinogenesis may be due to IkappaB-beta and IkappaB-alpha degradation, mainly IkappaB-beta degradation, which contributes to gene transcription related to proliferation required for neoplastic progression.
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