Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Sep 15;7(10):7242-8.
eCollection 2014.

Dysregulation of JAM-A plays an important role in human tumor progression

Chen Zhao  1 , Funian Lu  1 , Hongxia Chen  1 , Xianda Zhao  1 , Jun Sun  2 , Honglei Chen  1
Affiliations
Review

Dysregulation of JAM-A plays an important role in human tumor progression

Chen Zhao et al. Int J Clin Exp Pathol. .

Abstract

Junctional adhesion molecule A (JAM-A) is a transmembrane protein that belongs to the immunoglobulin (Ig) superfamily. Evidence determines that JAM-A plays a role in numerous cellular processes, including tight junction assembly, leukocyte migration, platelet activation, angiogenesis and virus binding. Recent research suggests that JAM-A is dysregulated in various cancers and is vital for tumor progression. JAM-A is implicated in carcinogenesis via different signal pathways such as TGF-β1 signaling. Furthermore, JAM-A expression in cancers is usually associated with certain outcome of patients and might be a prognostic indicator. In this review, the correlation between JAM-A expression and human cancers will be described.

Keywords: Tight junction; junctional adhesion molecule-A; tumor progression.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Cellular location and basic structure of JAM-A. JAM-A is component of TJ and located along the lateral membrane. JAM-A has two extracellular immunoglobulin-like domains, a single transmembrane segment and a cytoplasmic tail.
Figure 2
Figure 2
Dysregulation of JAM-A expression is required for cancer cell metastasis. Damage of JAM-A function contributes to tumor progression. In cancer cells, JAM-A overexpression (a) or underexpression (b) is related to increased migration and invasion.
See this image and copyright information in PMC

References

    1. Runkle EA, Mu D. Tight junction proteins: from barrier to tumorigenesis. Cancer Lett. 2013;337:41–48. - PMC - PubMed
    1. Chiba H, Osanai M, Murata M, Kojima T, Sawada N. Transmembrane proteins of tight junctions. Biochim Biophys Acta. 2008;1778:588–600. - PubMed
    1. Sawada N. Tight junction-related human diseases. Pathol Int. 2013;63:1–12. - PMC - PubMed
    1. Martìn-Padura I, Lostaglio S, Schneemann M, Williams L, Romano M, Fruscella P, Panzeri C, Stoppacciaro A, Ruco L, Villa A. Junctional adhesion molecule, a novel member of the immunoglobulin superfamily that distributes at intercellular junctions and modulates monocyte transmigration. J Cell Biol. 1998;142:117–127. - PMC - PubMed
    1. Williams L, Martin-Padura I, Dejana E, Hogg N, Simmons D. Identification and characterisation of human junctional adhesion molecule (JAM) Mol Immunol. 1999;36:1175–1188. - PubMed

Publication types

LinkOut - more resources