Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 22, Issue 8, Pages 1121-1134Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E10-10-0845
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Funding
- Crohn's and Colitis Foundation of America
- AGA Foundation for Digestive Health and Nutrition
- National Institutes of Health [DK-61739, DK-55679, DK-59888]
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Desmocollin-2 (Dsc2) and desmoglein-2 (Dsg2) are transmembrane cell adhesion proteins of desmosomes. Reduced expression of Dsc2 has been reported in colorectal carcinomas, suggesting that Dsc2 may play a role in the development and/or progression of colorectal cancer. However, no studies have examined the mechanistic contribution of Dsc2 deficiency to tumorigenesis. Here we report that loss of Dsc2 promotes cell proliferation and enables tumor growth in vivo through the activation of Akt/beta-catenin signaling. Inhibition of Akt prevented the increase in beta-catenin-dependent transcription and proliferation following Dsc2 knockdown and attenuated the in vivo growth of Dsc2-deficient cells. Taken together, our results provide evidence that loss of Dsc2 contributes to the growth of colorectal cancer cells and highlight a novel mechanism by which the desmosomal cadherins regulate beta-catenin signaling.
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