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About the Authors:
Petra A. Tsuji
* E-mail: [email protected]
Affiliations Department of Biological Sciences, Towson University, Towson, Maryland, United States of America, Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, National Institutes of Health, Bethesda, Maryland, United States of America
Bradley A. Carlson
Affiliation: Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, National Institutes of Health, Bethesda, Maryland, United States of America
Salvador Naranjo-Suarez
Affiliation: Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, National Institutes of Health, Bethesda, Maryland, United States of America
Min-Hyuk Yoo
Affiliation: Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, National Institutes of Health, Bethesda, Maryland, United States of America
Xue-Ming Xu
Affiliation: Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, National Institutes of Health, Bethesda, Maryland, United States of America
Dmitri E. Fomenko
Affiliation: Department of Biochemistry, University of Nebraska, Lincoln, Nebraska, United States of America
Vadim N. Gladyshev
Affiliation: Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
Dolph L. Hatfield
Affiliation: Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, National Institutes of Health, Bethesda, Maryland, United States of America
Cindy D. Davis
Affiliation: Office of Dietary Supplements, National Institutes of Health, Bethesda, Maryland, United States of America
Introduction
Colorectal cancer remains the second leading cause of cancer-related deaths in the United States with an estimated 51,690 deaths (26,470 in men and 25,220 in women) during 2012 [1]. Aberrant colonic crypts and aberrant crypt foci are putative pre-neoplastic colon lesions, and are considered good biomarkers for determining colorectal cancer risk, as the number of pre-neoplastic lesions is statistically associated with the number of tumors that ultimately develop [2], [3]. There is evidence from epidemiologic, clinical and preclinical studies that dietary supplementation with the essential trace mineral selenium reduces the incidence and mortality of colon cancer in humans [4], [5]. Previous animal studies have demonstrated protective effects of selenium fortification against aberrant crypt formation and colon tumor development [5]–[8]. Recent studies indicate that both low molecular weight selenocompounds and selenium-containing proteins (selenoproteins) can mediate the cancer-protective effects of selenium in the colon [9].
Selenium is incorporated into selenoproteins as the 21st amino acid selenocysteine [10], and there are 24 known selenoprotein genes in mice [11]. One of the more abundant...