RGD Reference Report - Abrogation of junctional adhesion molecule-A expression induces cell apoptosis and reduces breast cancer progression. - Rat Genome Database

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Abrogation of junctional adhesion molecule-A expression induces cell apoptosis and reduces breast cancer progression.

Authors: Murakami, M  Giampietro, C  Giannotta, M  Corada, M  Torselli, I  Orsenigo, F  Cocito, A  D'Ario, G  Mazzarol, G  Confalonieri, S  Di Fiore, PP  Dejana, E 
Citation: Murakami M, etal., PLoS One. 2011;6(6):e21242. doi: 10.1371/journal.pone.0021242. Epub 2011 Jun 17.
RGD ID: 7488916
Pubmed: PMID:21695058   (View Abstract at PubMed)
PMCID: PMC3117883   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0021242   (Journal Full-text)

Intercellular junctions promote homotypic cell to cell adhesion and transfer intracellular signals which control cell growth and apoptosis. Junctional adhesion molecule-A (JAM-A) is a transmembrane immunoglobulin located at tight junctions of normal epithelial cells of mammary ducts and glands. In the present paper we show that JAM-A acts as a survival factor for mammary carcinoma cells. JAM-A null mice expressing Polyoma Middle T under MMTV promoter develop significantly smaller mammary tumors than JAM-A positive mice. Angiogenesis and inflammatory or immune infiltrate were not statistically modified in absence of JAM-A but tumor cell apoptosis was significantly increased. Tumor cells isolated from JAM-A null mice or 4T1 cells incubated with JAM-A blocking antibodies showed reduced growth and increased apoptosis which paralleled altered junctional architecture and adhesive function. In a breast cancer clinical data set, tissue microarray data show that JAM-A expression correlates with poor prognosis. Gene expression analysis of mouse tumor samples showed a correlation between genes enriched in human G3 tumors and genes over expressed in JAM-A +/+ mammary tumors. Conversely, genes enriched in G1 human tumors correlate with genes overexpressed in JAM-A-/- tumors. We conclude that down regulation of JAM-A reduces tumor aggressive behavior by increasing cell susceptibility to apoptosis. JAM-A may be considered a negative prognostic factor and a potential therapeutic target.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Animal Mammary Neoplasms  ISOF11r (Mus musculus)7488916; 7488916 RGD 
Animal Mammary Neoplasms  IMP 7488916 RGD 

Objects Annotated

Genes (Rattus norvegicus)
F11r  (F11 receptor)

Genes (Mus musculus)
F11r  (F11 receptor)

Genes (Homo sapiens)
F11R  (F11 receptor)


Additional Information