Linked Life Data

18202022

Source:http://linkedlifedata.com/resource/pubmed/id/18202022

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-1-18
pubmed:abstractText
3,4-dihydroxybenzalacetone (DBL) is a polyphenol derived from the medicinal plant Chaga [Inonotus obliquus (persoon) Pilat]. Although Chaga is used in Russia folk medicine to treat tumors, very little is known about its mechanism of action. Because most genes involved in inflammation, antiapoptosis, and cell proliferation are regulated by the transcription factor nuclear factor-kappaB (NF-kappaB), we postulated that DBL activity is mediated via modulation of the NF-kappaB activation pathway. We investigated the effects of DBL on NF-kappaB activation by electrophoretic mobility shift assay and on NF-kappaB-regulated gene expression by Western blot analysis. We found that DBL suppressed NF-kappaB activation by a wide variety of inflammatory agents, including tumor necrosis factor (TNF), interleukin-1beta, epidermal growth factor, okadaic acid, phorbol 12-myristate 13-acetate, and lipopolysaccharide. The suppression was not cell type specific and inhibited both inducible and constitutive NF-kappaB activation. DBL did not interfere with the binding of NF-kappaB to DNA but rather inhibited IkappaBalpha kinase activity, IkappaBalpha phosphorylation and degradation, p65 phosphorylation, and translocation. DBL also suppressed the expression of TNF-induced and NF-kappaB-regulated proliferative, antiapoptotic, and metastatic gene products. These effects correlated with enhancement of TNF-induced apoptosis and suppression of TNF-induced invasion. Together, our results indicate that DBL inhibits NF-kappaB activation and NF-kappaB-regulated gene expression, which may explain the ability of DBL to enhance apoptosis and inhibit invasion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1535-7163
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
191-201
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18202022-Active Transport, Cell Nucleus, pubmed-meshheading:18202022-Antineoplastic Agents, pubmed-meshheading:18202022-Apoptosis, pubmed-meshheading:18202022-Cell Line, Tumor, pubmed-meshheading:18202022-Cell Proliferation, pubmed-meshheading:18202022-DNA, pubmed-meshheading:18202022-Enzyme Activation, pubmed-meshheading:18202022-Flavonoids, pubmed-meshheading:18202022-Gene Expression Regulation, Neoplastic, pubmed-meshheading:18202022-Humans, pubmed-meshheading:18202022-I-kappa B Kinase, pubmed-meshheading:18202022-Molecular Structure, pubmed-meshheading:18202022-NF-kappa B, pubmed-meshheading:18202022-Neoplasm Invasiveness, pubmed-meshheading:18202022-Neoplasms, pubmed-meshheading:18202022-Phenols, pubmed-meshheading:18202022-Phosphorylation, pubmed-meshheading:18202022-Polyphenols, pubmed-meshheading:18202022-Protein Binding, pubmed-meshheading:18202022-Protein Kinase Inhibitors, pubmed-meshheading:18202022-Time Factors, pubmed-meshheading:18202022-Tumor Necrosis Factors
pubmed:year
2008
pubmed:articleTitle
Identification of a novel blocker of IkappaBalpha kinase activation that enhances apoptosis and inhibits proliferation and invasion by suppressing nuclear factor-kappaB.
pubmed:affiliation
Cytokine Research Section, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Unit 143, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural