Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-2-4
pubmed:abstractText
High levels of the cyclooxygenase-2 (COX-2) protein have been associated with invasion and metastasis of breast tumors. Both prostaglandin E(2) (PGE(2)) and interleukin-8 (IL-8) have been shown to mediate the invasive activity of COX-2 in breast cancer cells. Here we expand these studies to determine how COX-2 uses PGE(2) and IL-8 to induce breast cancer cell invasion. We demonstrated that PGE(2) and IL-8 decreased the expression of the tumor suppressor protein Programmed Cell Death 4 (PDCD4). We hypothesized that suppression of PDCD4 expression is vital to the invasive activity of PGE(2) and IL-8. In MCF-7 cells overexpressing PDCD4 (MCF-7/PDCD4), PGE(2) and IL-8 failed to induce invasion, in contrast to the parental MCF-7 cells, thus indicating that PDCD4 blocks breast cancer cell invasion. MCF-7/PDCD4 cells produced higher levels of the Tissue Inhibitor of Metalloproteinases-2 (TIMP-2) than the parental cells. Silencing TIMP-2 mRNA in MCF-7/PDCD4 cells reversed the anti-invasive effects of PDCD4, allowing PGE(2) and IL-8 to induce the invasion of these cells. Here we report the novel findings that suppression of PDCD4 expression is vital for the invasive activity of COX-2 mediated by PGE(2) and IL-8, and that PDCD4 increases TIMP-2 expression to inhibit breast cancer cell invasion.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-10570194, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-11135226, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-11314000, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-11402303, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-11494140, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-11830510, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-11948407, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-12482958, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-12784332, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-12898601, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-14985450, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-15050733, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-15317660, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-15809733, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-16024603, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-16127422, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-16274040, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-16449643, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-16682950, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-16831226, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17053147, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17143488, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17259349, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17297470, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17332916, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17342087, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17828298, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17849461, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17982621, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-17991735, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-9153295, http://linkedlifedata.com/resource/pubmed/commentcorrection/18386173-9815852
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1573-7217
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
114
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
203-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:18386173-Apoptosis Regulatory Proteins, pubmed-meshheading:18386173-Blotting, Western, pubmed-meshheading:18386173-Breast Neoplasms, pubmed-meshheading:18386173-Cyclooxygenase 2, pubmed-meshheading:18386173-Dinoprostone, pubmed-meshheading:18386173-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:18386173-Female, pubmed-meshheading:18386173-Gene Expression, pubmed-meshheading:18386173-Gene Expression Regulation, Neoplastic, pubmed-meshheading:18386173-Humans, pubmed-meshheading:18386173-Interleukin-8, pubmed-meshheading:18386173-Neoplasm Invasiveness, pubmed-meshheading:18386173-RNA, Messenger, pubmed-meshheading:18386173-RNA, Small Interfering, pubmed-meshheading:18386173-RNA Interference, pubmed-meshheading:18386173-RNA-Binding Proteins, pubmed-meshheading:18386173-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18386173-Tissue Inhibitor of Metalloproteinase-2, pubmed-meshheading:18386173-Tumor Cells, Cultured
pubmed:year
2009
pubmed:articleTitle
Programmed cell death 4 inhibits breast cancer cell invasion by increasing tissue inhibitor of metalloproteinases-2 expression.
pubmed:affiliation
Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Unit 422, Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural