RGD Reference Report - JAM-A expression positively correlates with poor prognosis in breast cancer patients. - Rat Genome Database

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JAM-A expression positively correlates with poor prognosis in breast cancer patients.

Authors: McSherry, EA  McGee, SF  Jirstrom, K  Doyle, EM  Brennan, DJ  Landberg, G  Dervan, PA  Hopkins, AM  Gallagher, WM 
Citation: McSherry EA, etal., Int J Cancer. 2009 Sep 15;125(6):1343-51. doi: 10.1002/ijc.24498.
RGD ID: 7488915
Pubmed: PMID:19533747   (View Abstract at PubMed)
DOI: DOI:10.1002/ijc.24498   (Journal Full-text)

The cell-cell adhesion protein junctional adhesion molecule-A (JAM-A) influences epithelial cell morphology and migration. As migration is required for tumor cell invasion and metastasis, we sought to elucidate the role of JAM-A in invasive breast cancer. A breast cancer tissue microarray was analyzed for JAM-A protein expression, in parallel with analysis of JAM-A gene expression data from a breast cancer clinical dataset. Our data demonstrate a novel association between JAM-A gene and protein upregulation and poor prognosis in breast cancer. To mechanistically dissect this process, we used lentiviral technology to stably knock down JAM-A gene expression by shRNA in MCF7 breast cancer cells, which express high-endogenous levels of JAM-A. We also antagonized JAM-A function in wild-type MCF7 cells using an inhibitory antibody that blocks JAM-A dimerization. Knockdown or functional antagonism of JAM-A decreased breast cancer cell migration in scratch-wound assays. Reductions in beta1-integrin protein levels were observed after JAM-A-knockdown in MCF7 cells, suggesting a mechanism for reduced motility after loss of JAM-A. Consistent with this hypothesis, tissue microarray analysis of beta1-integrin protein expression in invasive breast cancer tissues revealed a trend toward high beta1-integrin protein levels being indicative of poor prognosis. Twenty-two percent of patients were observed to coexpress high levels of JAM-A and beta1-integrin protein, and MDA-MB-231 breast cells stably overexpressing JAM-A showed an increase in beta1-integrin protein expression. Our results are consistent with a previously unreported role for JAM-A overexpression as a possible mechanism contributing to progression in primary breast cancer; and a potential therapeutic target.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
breast cancer disease_progressionIEP 7488915 RGD 
breast cancer disease_progressionISOF11R (Homo sapiens)7488915; 7488915 RGD 

Objects Annotated

Genes (Rattus norvegicus)
F11r  (F11 receptor)

Genes (Mus musculus)
F11r  (F11 receptor)

Genes (Homo sapiens)
F11R  (F11 receptor)


Additional Information