Source:http://linkedlifedata.com/resource/pubmed/id/16158054
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-1-13
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pubmed:abstractText |
The c-jun oncogene is frequently overexpressed in non-small-cell lung cancers (NSCLC), but its functional involvement in lung cancer development has not been clearly elucidated. In this study, we found that among the immediate-early serum responsible genes, exemplified by c-jun, c-fos and c-myc, induction of c-jun in a human bronchial epithelial cell line, BEAS-2B, was dependent on anchorage, in contrast to clear induction of c-fos and c-myc under both anchorage-dependent and -independent conditions. In fact, forced expression of c-jun in BEAS-2B cells significantly increased cell viability and colony formation in soft agar. Furthermore, we also found that such anchorage-dependent regulation of c-jun was lost in a significant fraction of human lung cancer cell lines. Interestingly, suppressed anchorage-independent but not anchorage-dependent growth was noted by constitutive expression of a dominant-negative c-jun mutant in a lung cancer cell line showing dysregulated and sustained c-jun expression in the absence of anchorage. These findings suggest that dysregulated c-jun expression may be involved in the acquisition of anchorage independence in the process of human lung carcinogenesis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin A,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-fos,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-myc,
http://linkedlifedata.com/resource/pubmed/chemical/Stathmin
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0950-9232
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
12
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
271-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16158054-Bronchi,
pubmed-meshheading:16158054-Cell Adhesion,
pubmed-meshheading:16158054-Cell Proliferation,
pubmed-meshheading:16158054-Cell Survival,
pubmed-meshheading:16158054-Colony-Forming Units Assay,
pubmed-meshheading:16158054-Cyclin A,
pubmed-meshheading:16158054-Epithelial Cells,
pubmed-meshheading:16158054-Gene Expression Regulation,
pubmed-meshheading:16158054-Genes, Dominant,
pubmed-meshheading:16158054-Genes, ras,
pubmed-meshheading:16158054-Humans,
pubmed-meshheading:16158054-Lung Neoplasms,
pubmed-meshheading:16158054-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:16158054-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:16158054-Proto-Oncogene Proteins c-myc,
pubmed-meshheading:16158054-Social Control, Formal,
pubmed-meshheading:16158054-Stathmin
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pubmed:year |
2006
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pubmed:articleTitle |
Altered regulation of c-jun and its involvement in anchorage-independent growth of human lung cancers.
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pubmed:affiliation |
Division of Molecular Carcinogenesis, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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