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Updated: Jun 3, 2026
10:37
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
JAM-A regulates epithelial proliferation through Akt/β-catenin signalling
Porfirio Nava1, Christopher T Capaldo, Stefan Koch
1Epithelial Pathobiology Research Unit, Department of Pathology, Emory University, Whitehead Biomedical Research Building, Room 105E, 615 Michael Street, Atlanta, Georgia 30322, USA.
EMBO Reports
|March 5, 2011
Summary
Junctional adhesion molecule-A (JAM-A) restricts intestinal epithelial cell proliferation by inhibiting Akt-dependent β-catenin activation. This discovery reveals a new role for JAM-A in maintaining intestinal homeostasis.
Area of Science:
- Cell biology
- Gastroenterology
- Oncology
Background:
- Junctional adhesion molecule-A (JAM-A) expression correlates with tumor progression.
- A direct role for JAM-A in regulating cell proliferation remains unestablished.
Purpose of the Study:
- To investigate the direct role of JAM-A in regulating intestinal epithelial cell (IEC) proliferation.
- To elucidate the molecular mechanisms by which JAM-A influences IEC proliferation and homeostasis.
Main Methods:
- Utilized complementary in vivo and in vitro experimental approaches.
- Employed transgenic JAM-A(-/-)/β-catenin/T-cell factor reporter mice.
- Investigated the effects of Akt inhibition on colonic crypts in JAM-A-deficient mice.
Main Results:
- Demonstrated that JAM-A restricts IEC proliferation in a dimerization-dependent manner.
- Showed that JAM-A inhibits Akt-dependent β-catenin activation.
- Observed enhanced β-catenin-dependent transcription in JAM-A-deficient IECs.
- Confirmed that Akt inhibition reversed colonic crypt hyperproliferation in JAM-A-deficient mice.
Conclusions:
- Established a novel inhibitory role for JAM-A in IEC proliferation.
- Linked JAM-A function to the regulation of Akt/β-catenin signaling pathway.
- Identified a new mechanism regulating intestinal epithelial homeostasis involving JAM-A.
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