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J Cancer. 2016 Jan 01;7(2):174-83. doi: 10.7150/jca.13387. eCollection 2016.

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

Journal of Cancer

Kamal Datta, Shubhankar Suman, Santosh Kumar, Albert J Fornace

Affiliations

  1. 1. Department of Biochemistry and Molecular & Cellular Biology and Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC USA.
  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.

PMID: 26819641 PMCID: PMC4716850 DOI: 10.7150/jca.13387

Abstract

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/+; HZE-particles; High-LET radiation; Intestinal tumor; Proteasome; Space radiation; Tumorigenesis; β-catenin

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