J Cancer 2016; 7(2):174-183. doi:10.7150/jca.13387 This issue


Colorectal Carcinogenesis, Radiation Quality, and the Ubiquitin-Proteasome Pathway

Kamal Datta1✉, Shubhankar Suman1, Santosh Kumar1, Albert J Fornace Jr.1, 2

1. Department of Biochemistry and Molecular & Cellular Biology and Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC USA.
2. Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia

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Datta K, Suman S, Kumar S, Fornace AJ Jr.. Colorectal Carcinogenesis, Radiation Quality, and the Ubiquitin-Proteasome Pathway. J Cancer 2016; 7(2):174-183. doi:10.7150/jca.13387. Available from https://www.jcancer.org/v07p0174.htm

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Adult colorectal epithelium undergoes continuous renewal and maintains homeostatic balance through regulated cellular proliferation, differentiation, and migration. The canonical Wnt signaling pathway involving the transcriptional co-activator β-catenin is important for colorectal development and normal epithelial maintenance, and deregulated Wnt/β-catenin signaling has been implicated in colorectal carcinogenesis. Colorectal carcinogenesis has been linked to radiation exposure, and radiation has been demonstrated to alter Wnt/β-catenin signaling, as well as the proteasomal pathway involved in the degradation of the signaling components and thus regulation of β-catenin. The current review discusses recent progresses in our understanding of colorectal carcinogenesis in relation to different types of radiation and roles that radiation quality plays in deregulating β-catenin and ubiquitin-proteasome pathway (UPP) for colorectal cancer initiation and progression.

Keywords: APCMin/+, Intestinal tumor, Space radiation, High-LET radiation, Tumorigenesis, Proteasome, β-catenin, HZE-particles