Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
30
pubmed:dateCreated
2011-7-28
pubmed:abstractText
Lung cancer is the most common cause of cancer-related mortality worldwide. Here, we report elevated expression of tribbles homolog 2 (TRIB2) in primary human lung tumors and in non-small cell lung cancer cells that express low levels of differentiation-inducing transcription factor CCAAT/enhancer-binding protein alpha (C/EBP?). In approximately 10-20% of cases, elevated TRIB2 expression resulted from gene amplification. TRIB2 knockdown was found to inhibit cell proliferation and in vivo tumor growth. In addition, TRIB2 knockdown led to morphological changes similar to C/EBP? overexpression and correlated with increased expression and activity of C/EBP?. TRIB2-mediated regulation of C/EBP? was found to occur through the association of TRIB2 with the E3 ligase TRIM21. Together, these data identify TRIB2 as a potential driver of lung tumorigenesis through a mechanism that involves downregulation of C/EBP?.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1476-5594
pubmed:author
pubmed:issnType
Electronic
pubmed:day
28
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3328-35
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Overexpression of TRIB2 in human lung cancers contributes to tumorigenesis through downregulation of C/EBP?.
pubmed:affiliation
Genomics Institute of the Novartis Research Foundation, San Diego, CA 92121, USA. bgrandinetti@gnf.org
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural