Linked Life Data

19551863

Source:http://linkedlifedata.com/resource/pubmed/id/19551863

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2009-10-5
pubmed:abstractText
Id-1 (inhibitor of differentiation or DNA binding) is a helix-loop-helix protein that is overexpressed in many types of cancer including esophageal squamous cell carcinoma (ESCC). We previously reported that ectopic Id-1 expression activates the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in human esophageal cancer cells. In this study, we confirmed a positive correlation between Id-1 and phospho-AKT (Ser473) expressions in ESCC cell lines, as well as in ESCC on a tissue microarray. To investigate the significance of Id-1 in esophageal cancer progression, ESCC cells with stable ectopic Id-1 expression were inoculated subcutaneously into the flank of nude mice and were found to form larger tumors that showed elevated Ki-67 proliferation index and increased angiogenesis, as well as reduced apoptosis, compared with control cells expressing the empty vector.The Id-1-overexpressing cells also exhibited enhanced metastatic potential in the experimental metastasis assay. Treatment with the PI3K inhibitor LY294002 attenuated the tumor promotion effects of Id-1, indicating that the effects were mediated by the PI3K/AKT signaling pathway. In addition, our in vitro experiments showed that ectopic Id-1 expression altered the expression levels of markers associated with epithelial-mesenchymal transition and enhanced the migration ability of esophageal cancer cells. The Id-1-overexpressing ESCC cells also exhibited increased invasive potential, which was in part due to PI3K/AKT-dependent modulation of matrix metalloproteinase-9 expression. In conclusion, our results provide the first evidence that Id-1 promotes tumorigenicity and metastasis of human esophageal cancer in vivo and that the PI3K inhibitor LY294002 can attenuate these effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1097-0215
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2576-85
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:19551863-Animals, pubmed-meshheading:19551863-Apoptosis, pubmed-meshheading:19551863-Blotting, Western, pubmed-meshheading:19551863-Carcinoma, Squamous Cell, pubmed-meshheading:19551863-Cell Movement, pubmed-meshheading:19551863-Cell Proliferation, pubmed-meshheading:19551863-Esophageal Neoplasms, pubmed-meshheading:19551863-Female, pubmed-meshheading:19551863-Fluorescent Antibody Technique, pubmed-meshheading:19551863-Humans, pubmed-meshheading:19551863-Immunoenzyme Techniques, pubmed-meshheading:19551863-Inhibitor of Differentiation Protein 1, pubmed-meshheading:19551863-Mice, pubmed-meshheading:19551863-Mice, Inbred BALB C, pubmed-meshheading:19551863-Mice, Nude, pubmed-meshheading:19551863-Neoplasm Invasiveness, pubmed-meshheading:19551863-Phosphatidylinositol 3-Kinases, pubmed-meshheading:19551863-Proto-Oncogene Proteins c-akt, pubmed-meshheading:19551863-Signal Transduction, pubmed-meshheading:19551863-Tumor Cells, Cultured, pubmed-meshheading:19551863-Wound Healing, pubmed-meshheading:19551863-Xenograft Model Antitumor Assays
pubmed:year
2009
pubmed:articleTitle
Id-1 promotes tumorigenicity and metastasis of human esophageal cancer cells through activation of PI3K/AKT signaling pathway.
pubmed:affiliation
Cancer Biology Group, Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't