title: Quantitative proteomic analysis reveals that anti-cancer effects of selenium-binding protein 1 in vivo are associated with metabolic pathways.
abstract: Previous studies have shown the tumor-suppressive role of selenium-binding protein 1 (SBP1), but the underlying mechanisms are unclear. In this study, we found that induction of SBP1 showed significant inhibition of colorectal cancer cell growth and metastasis in mice. We further employed isobaric tags for relative and absolute quantitation (iTRAQ) to identify proteins that were involved in SBP1-mediated anti-cancer effects in tumor tissues. We identified 132 differentially expressed proteins, among them, 53 proteins were upregulated and 79 proteins were downregulated. Importantly, many of the differentially altered proteins were associated with lipid/glucose metabolism, which were also linked to Glycolysis, MAPK, Wnt, NF-kB, NOTCH and epithelial-mesenchymal transition (EMT) signaling pathways. These results have revealed a novel mechanism that SBP1-mediated cancer inhibition is through altering lipid/glucose metabolic signaling pathways.
authors.affiliation: College of Food Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China; Department of Pathology, Xinxiang Medical University, Xinxiang, 453003, China; Department of Pathology, University of Illinois at Chicago, Chicago, Illinois 60612, United States of America.
authors.forename: Qi
authors.initials: Q
authors.lastname: Ying
authors.affiliation: Department of Pathology, University of Illinois at Chicago, Chicago, Illinois 60612, United States of America.
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Ansong
authors.affiliation: Department of Pathology, University of Illinois at Chicago, Chicago, Illinois 60612, United States of America.
authors.forename: Alan M
authors.initials: AM
authors.lastname: Diamond
authors.affiliation: College of Food Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.
authors.forename: Zhaoxin
authors.initials: Z
authors.lastname: Lu
authors.affiliation: Department of Pathology, Xinxiang Medical University, Xinxiang, 453003, China; Department of Pathology, University of Illinois at Chicago, Chicago, Illinois 60612, United States of America.
authors.forename: Wancai
authors.initials: W
authors.lastname: Yang
authors.affiliation: College of Food Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Bie
mesh_terms: D000818:Animals; D003106:Colon / Q000378:metabolism / Q000473:pathology*; D003110:Colonic Neoplasms / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D045325:HCT116 Cells; D006801:Humans; D050356:Lipid Metabolism; D053858:Metabolic Networks and Pathways; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009362:Neoplasm Metastasis / Q000473:pathology; D040901:Proteomics / Q000379:methods; D051137:Selenium-Binding Proteins / Q000032:analysis / Q000378:metabolism*
chemical_list: C495175:SELENBP1 protein, human; C495176:Selenbp1 protein, mouse; D051137:Selenium-Binding Proteins; D005947:Glucose