Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2010-11-24
pubmed:abstractText
Krüppel-Like Factor 4 (KLF4) functions as a tumor suppressor in some cancers, but its molecular mechanism is not clear. Our recent study also showed that the expression of KLF4 is dramatically reduced in primary lung cancer tissues. To investigate the possible role of KLF4 in lung cancer, we stably transfected KLF4 into cells from lung cancer cell lines H322 and A549 to determine the cells' invasion ability. Our results showed that ectopic expression of KLF4 extensively suppressed lung cancer cell invasion in Matrigel. This effect was independent of KLF4-mediated p21 up-regulation because ectopic expression of p21 had minimal effect on cell invasion. Our analysis of the expression of 12 genes associated with cell invasion in parental, vector-transfected, and KLF4-transfected cells showed that ectopic expression of KLF4 resulted in extensively repressed expression of secreted protein acidic and rich in cysteine (SPARC), an extracellular matrix protein that plays a role in tumor development and metastasis. Knockdown of SPARC expression in H322 and A549 cells led to suppression of cell invasion, comparable to that observed in KLF4-transfected cells. Moreover, retrovirus-mediated restoration of SPARC expression in KLF4-transfected cells abrogated KLF4-induced anti-invasion activity. Together, our results indicate that KLF4 inhibits lung cancer cell invasion by suppressing SPARC gene expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/CDKN1A protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Collagen, http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor..., http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations, http://linkedlifedata.com/resource/pubmed/chemical/GKLF protein, http://linkedlifedata.com/resource/pubmed/chemical/Kruppel-Like Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/Laminin, http://linkedlifedata.com/resource/pubmed/chemical/Osteonectin, http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering, http://linkedlifedata.com/resource/pubmed/chemical/matrigel
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1555-8576
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
507-13
pubmed:dateRevised
2011-11-1
pubmed:meshHeading
pubmed-meshheading:20215880-Blotting, Western, pubmed-meshheading:20215880-Cell Adhesion, pubmed-meshheading:20215880-Cell Movement, pubmed-meshheading:20215880-Cell Proliferation, pubmed-meshheading:20215880-Collagen, pubmed-meshheading:20215880-Cyclin-Dependent Kinase Inhibitor p21, pubmed-meshheading:20215880-Drug Combinations, pubmed-meshheading:20215880-Gene Expression Regulation, Neoplastic, pubmed-meshheading:20215880-Humans, pubmed-meshheading:20215880-Kruppel-Like Transcription Factors, pubmed-meshheading:20215880-Laminin, pubmed-meshheading:20215880-Lung Neoplasms, pubmed-meshheading:20215880-Neoplasm Invasiveness, pubmed-meshheading:20215880-Osteonectin, pubmed-meshheading:20215880-Proteoglycans, pubmed-meshheading:20215880-RNA, Messenger, pubmed-meshheading:20215880-RNA, Small Interfering, pubmed-meshheading:20215880-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20215880-Transfection, pubmed-meshheading:20215880-Tumor Cells, Cultured, pubmed-meshheading:20215880-Up-Regulation
pubmed:year
2010
pubmed:articleTitle
KLF4 inhibition of lung cancer cell invasion by suppression of SPARC expression.
pubmed:affiliation
Department of Pulmonary Medicine, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural