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Updated: May 12, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
DDB2 suppresses epithelial-to-mesenchymal transition in colon cancer
Nilotpal Roy1, Prashant V Bommi, Uppoor G Bhat
1Department of Biochemistry and Molecular Genetics; Center of Molecular Biology of Oral Diseases College of Dentistry, Cancer Center; and Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.
Abstract:
Colon cancer is one of the deadliest cancers worldwide because of its metastasis to other essential organs. Metastasis of colon cancer involves a complex set of events, including epithelial-to-mesenchymal transition (EMT) that increases invasiveness of the tumor cells. Here, we show that the xeroderma pigmentosum group E (XPE) gene product, damaged DNA-binding protein (DDB)-2, is downregulated in high-grade colon cancers, and it plays a dominant role in the suppression of EMT of the colon cancer cells. Depletion of DDB2 promotes mesenchymal phenotype, whereas expression of DDB2 promotes epithelial phenotype. DDB2 constitutively represses genes that are the key activators of EMT, indicating that DDB2 is a master regulator of EMT of the colon cancer cells. Moreover, we observed evidence that DDB2 functions as a barrier for EMT induced by hypoxia and TGF-β. Also, we provide evidence that DDB2 inhibits metastasis of colon cancer. The results presented here identify a transcriptional regulatory pathway of DDB2 that is directly linked to the mechanisms that suppress metastasis of colon cancer.
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