Linked Life Data

11691825

Source:http://linkedlifedata.com/resource/pubmed/id/11691825

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
2001-11-5
pubmed:abstractText
To identify and understand early events in lung carcinogenesis, we used a cDNA array to screen for genes that are expressed differentially in normal human bronchial epithelial (NHBE) cells and a tumorigenic cell line (1170-I) derived from immortalized HBE cells after exposure to cigarette smoke condensate in vivo. Among these genes, we have identified the S100A2 gene, which encodes a nuclear calcium-binding protein, as being down-regulated in the 1170-I cells. Because this gene has been implicated as a tumor suppressor in breast cancer, we examined its potential role as a tumor suppressor in lung carcinogenesis. Levels of S100A2 transcript and protein, which were high in NHBE cells, decreased by up to 50% in immortalized HBE cells (BEAS-2B and 1799) and to low to nearly undetectable levels in transformed (1198) and tumorigenic (1170-I) HBE cells. Furthermore, S100A2 mRNA and protein were undetectable in 8 and expressed at a reduced level in 3 of 11 non-small cell lung cancer (NSCLC) cell lines. Positive immunohistochemical staining of S100A2 was detected in the majority (75-83%) of normal and hyperplastic lung tissues, whereas it was detected in <10% of metaplastic lung tissues, squamous cell carcinoma, and adenocarcinoma. Treatment of 1170-I HBE and NSCLC cells with 5-aza-2'-deoxycytidine resulted in partial restoration of S100A2 expression in seven of eight cell lines. Indeed, CpG methylation was detected in the promoter region of the S100A2 gene. Our results suggest that S100A2 expression is suppressed early during lung carcinogenesis, possibly by hypermethylation of its promoter, and that its loss may be a contributing factor in lung cancer development or a biomarker of early changes in this process.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7999-8004
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11691825-Animals, pubmed-meshheading:11691825-Antimetabolites, Antineoplastic, pubmed-meshheading:11691825-Azacitidine, pubmed-meshheading:11691825-Base Sequence, pubmed-meshheading:11691825-Bronchi, pubmed-meshheading:11691825-Carcinoma, Non-Small-Cell Lung, pubmed-meshheading:11691825-Cell Line, Transformed, pubmed-meshheading:11691825-Cell Transformation, Neoplastic, pubmed-meshheading:11691825-Chemotactic Factors, pubmed-meshheading:11691825-Epithelial Cells, pubmed-meshheading:11691825-Gene Expression Regulation, Neoplastic, pubmed-meshheading:11691825-Humans, pubmed-meshheading:11691825-Lung Neoplasms, pubmed-meshheading:11691825-Mice, pubmed-meshheading:11691825-Mice, Nude, pubmed-meshheading:11691825-Molecular Sequence Data, pubmed-meshheading:11691825-Neoplasm Staging, pubmed-meshheading:11691825-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:11691825-RNA, Neoplasm, pubmed-meshheading:11691825-Rats, pubmed-meshheading:11691825-S100 Proteins, pubmed-meshheading:11691825-Transplantation, Heterologous, pubmed-meshheading:11691825-Tumor Cells, Cultured, pubmed-meshheading:11691825-Tumor Markers, Biological
pubmed:year
2001
pubmed:articleTitle
Diminished expression of S100A2, a putative tumor suppressor, at early stage of human lung carcinogenesis.
pubmed:affiliation
Department of Thoracic/Head & Neck Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.