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Jam-a


Official Full Name
F11 receptor
Organism
Mus musculus
Gene ID
16456
Background
Predicted to enable PDZ domain binding activity; integrin binding activity; and protein homodimerization activity. Involved in intestinal absorption; regulation of cytokine production; and regulation of membrane permeability. Acts upstream of or within cell adhesion and epithelial cell differentiation. Located in bicellular tight junction. Is expressed in several structures, including 4-8 cell stage embryo; alimentary system; forebrain; sensory organ; and urinary system. Human ortholog(s) of this gene implicated in hypertension. Orthologous to human F11R (F11 receptor). [provided by Alliance of Genome Resources, Feb 2025]
Synonyms
F11r; JAM; Jcam; JAM-1; JAM-A; Jcam1; Ly106; ESTM33; 9130004G24

Cat.No. Product Name Price
SHH043247 shRNA set against Mouse F11r(NM_172647.2) Inquiry
SHH043211 shRNA set against Rat F11r(NM_053796.1) Inquiry
SHH043265 shRNA set against Human F11R(NM_016946.4) Inquiry
SHH288385 shRNA set against Human F11R (NM_016946.4) Inquiry
SHH288389 shRNA set against Rat F11R (NM_053796.1) Inquiry
SHW002624 shRNA set against Chicken F11R (NM_001083366) Inquiry
Cat.No. Product Name Price
CDFR013538 Rat F11r cDNA Clone(NM_053796.1) Inquiry
MiUTR1H-03359 F11R miRNA 3'UTR clone Inquiry
MiUTR1M-04533 F11R miRNA 3'UTR clone Inquiry
MiUTR1R-01794 F11R miRNA 3'UTR clone Inquiry
CDCB164099 Chicken F11R ORF Clone (NM_001083366) Inquiry
CDCB193224 Rabbit F11R ORF clone (XM_008264206.1) Inquiry
CDCL184132 Mouse F11R ORF clone(NM_172647.2) Inquiry
CDCL184133 Rat F11R ORF clone(NM_053796.1) Inquiry
CDCL185011 Human JAM-A ORF clone(NM_016946.4) Inquiry
CDCS414379 Human F11R ORF Clone (BC001533) Inquiry

Detailed Information

Recent research

Junctional adhesion molecule A (JAM-A), also known as F11R, JAM-1, or CD321, belongs to the immunoglobulin (Ig) superfamily of adhesion molecules, is a type I transmembrane immunoglobulin G glycoprotein. It is located in tight junction (TJ) and along the lateral membrane of endothelial and epithelial cells and is involved in the barrier function of TJs in both endothelial and epithelial cells, and development of apico-basal cell polarity in epithelial cells. The expression of JAM-A has been shown on the surface of endothelial and epithelial cells of various tissues as well as platelets and cells of the immune system. JAM-A participates in diverse cell-cell adhesion processes, such as angiogenesis, leukocyte migration, platelet activation, reovirus binding and TJ assembling (Figure 1).Some reports suggest that JAM-A is dysregulated in various cancers and is vital for tumor progression. JAM-A is involved in carcinogenesis through different signaling pathways such as TGF-β1 signaling.

JAM-A Figure 1. Dysregulation of JAM-A expression is required for cancer cell metastasis.

JAM-A and Malignancy

Cell migration is an early requirement for tumor metastasis. In order to metastasize, cancer cells must be removed from the primary tumor and then to a distant organ, with the potential to proliferate into a secondary tumor.TJ proteins contribute to tumor cell invasion, migration and adhesion. Dysregulation of JAM-A has been linked to proliferation and tumor progression.

JAM-A and Endometrial carcinoma

In endometrial carcinoma, JAM-A expression is negatively correlated with grade, myometrial invasion, or stage and low JAM-A expression is significantly associated with low overall survival rate and progression-free survival rate. Besides, in 3-dimensional epithelial cell culture, JAM-A expression was significantly higher in well-differentiated adenocarcinoma than in poorly differentiated adenocarcinoma. Therefore, the expression of JAM-A may be reduced in high-grade or advanced endometrial cancer.

JAM-A and Pancreatic cancer

Low levels of JAM-A expression is an independent prognostic marker for adverse clinical outcome and is linked to tumor aggressiveness in pancreatic cancer. Depletion of JAM-A is related to positive lymph node status, the presence of distant metastasis and tumor grade, which suggests it may be involved in tumor progression. Moreover, an important role of ZO-2, another member of the JAM-associated protein complex has participated in the pathogenesis on pancreatic cancer.

JAM-A and Testicular cancer

Some reports have shown that JAM-A is expressed on germ cells in normal testis, but only in spermatogonia and spermatocytes. Besides JAM-A, TJ proteins are disorganized in testicular cancer. The localization of JAM-A is disorganized in tubules with testicular carcinoma in situ (CIS) and there is an aberrant high expression of JAM-A in seminoma. The expression of JAM-A by seminoma cells may promote tumor cell migration and infiltration.

JAM-A and Melanoma

JAM-A inhibits melanoma transendothelial migration. It has been provided in melanoma that inhibition of JAM-A expression promotes the transmigration efficiency of the melanoma cell lines (SLM8 cells). While the inhibition of JAM-C protein diminishes the efficiency of the A375 cell line to cross the endothelial cells, which means that JAM proteins may play opposite roles in melanoma cells migration.

JAM-A and Renal cell cancer

JAM-A protein expression is significantly down-regulated in patients with clear cell renal cell carcinoma. Depletion of JAM-A is an early event in the development of renal cancer and increases the migration of renal cancer cells. Under-expression of JAM-A is associated with a more aggressive phenotype.

JAM-A and Lung cancer

JAM-A mRNA in squamous cell carcinoma is about the same level compared to lung parenchyma while lower than in bronchial cells. On the other side, JAM-A mRNA level in adenocarcinoma is higher than those in lung parenchyma but slightly lower than in bronchial cells. Some studies investigated JAM-A expression in the lung tumor and normal tissues, JAM-A over-expression is detected in lung cancer tissues compared to normal tissues.

In addition, some reports have shown that high expression of JAM-A is significantly associated with TNM stage, lymph node metastasis and shorten overall survival. Suppression of JAM-A expression induces cell cycle arrest in the G 1 -phase and inhibits lung cancer cell growth. It promotes non-small cell lung cancer (NSCLC) cells proliferation by modulation of cell cycle-related molecules.

JAM-A and Breast cancer

Breast cancer (BC) is the most common type of cancer in women. Its mortality is mainly due to distant metastasis. However, the role of JAM-A in tumor growth and dissemination remains controversial. It is reported that JAM-A expression is down-regulated in metastatic breast cancer. Expression of JAM-A is inversely correlated to the ability of the breast cancer cells to migrate in their study of tumor cell lines. Over-expression of JAM-A in highly migratory cells (MDA-MB-231 cells) affects their morphology and inhibits both migration and invasion through collagen gels.

Additionally, over-expression of JAM-A in breast cancer may increase cell motility via down-stream effects on β1-integrin, which is one of several proteins used by cells migration. One report shows that JAM-A knockdown or inhibition in breast cancer cells significantly decrease the activity of Rap1 GTPase, a known activator of β1-integrin as well as a regulator of cellular adhesion. This reveals a novel role for JAM-A in driving breast cancer cell migration via activation of Rap1 GTPase and β1-integrin.Moreover, JAM-A is co-expressed with HER2 and related to aggressive breast cancer phenotypes. It may regulate HER2 proteasomal degradation and activity, probably offering a promise as an important therapeutic target in HER2-positive breast cancers.

Conclusion

JAM-A plays an important role in a variety of cancers. JAM-A is a new emerging target in carcinogenesis and the influence of JAM-A on tumor development and progression is complex. The role of JAM-A in tumor progression may be regulated in a tissue-dependent manner. In the future, based on better understanding of the molecular mechanisms of regulation and functions, JAM-A may become a prognostic indicator and beneficial target in tumor therapy.

References:

  1. Zhao C, et al. Dysregulation of JAM-A plays an important role in human tumor progression. International Journal of Clinical & Experimental Pathology, 2014, 7(10):7242-8.
  2. Aydogan H Y. Interactive Effects of Common Haplotypes of Two Leukocyte Diapedesis-Related Genes, LFA-1 and JAM-A on Breast Cancer Risk. UHOD - UluslararasiHematoloji-OnkolojiDergisi, 2018, 28(1):45-52.
  3. Monteiro A C, et al. Trans-dimerization of JAM-A regulates Rap2 and is mediated by a domain that is distinct from the cis-dimerization interface. Molecular Biology of the Cell, 2014, 25(10):1574.
  4. Cao M, et al. MicroRNA-495 induces breast cancer cell migration by targeting JAM-A. Protein and Cell, 2014, 5(11):862-872.
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