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標題: Methylglyoxal displays colorectal cancer-promoting properties in the murine models of azoxymethane and CT26 isografts
作者: Lin, Jer-An
Wu, Chi-Hao
Yen, Gow-Chin
關鍵字: Carbonyl stress;Colon cancer;Inflammation;Methylglyoxal;Oxidative stress;Animals;Azoxymethane;Carcinogenesis;Carcinogens;Cell Line;Cholesterol, LDL;Colorectal Neoplasms;Disease Models, Animal;Humans;Inflammation;Male;Mice;Mice, Inbred BALB C;Mice, Inbred ICR;Oxidative Stress;Precancerous Conditions;Pyruvaldehyde;Transplantation, Isogeneic
Project: Free radical biology & medicine, Volume 115, Page(s) 436-446.
Methylglyoxal (MG), a highly reactive carbonyl species (RCS) with pro-oxidant and proinflammatory properties, may be a colon tumor-promoting factor in food and biological systems. In the present study, we found that consumption of MG significantly deteriorated azoxymethane (AOM)-induced colonic preneoplastic lesions in ICR mice, in which biomarkers of oxidative stress and inflammation within the body and feces induced by MG-fueled carbonyl stress may have played important roles. Interestingly, exposure to MG also led to increases in the serum low-density lipoprotein (LDL)/high-density lipoprotein (HDL) ratio and fecal bile acid levels in mice, which may be critical factors involved in MG-induced colonic lesions. Additionally, MG treatment (50mg/kg body weight (BW); intraperitoneally) promoted tumor growth of CT26 isografts in mice partly by carbonyl stress-evoked protumorigenic responses, including low-grade inflammation and oxidative stress. Furthermore, primary tumor cells isolated from mice with MG-induced CT26 isografts had greater proliferative and migratory activities as well as stem-like properties compared to those isolated from the vehicle controls. Excitingly, enhanced expression or activation of proteins that modulate cell survival, proliferation, or migration/invasion was also observed in those cells. In conclusion, it is conceivable that MG-induced carbonyl stress may be the pivotal promoter involved in colon cancer progression.
DOI: 10.1016/j.freeradbiomed.2017.12.020
Appears in Collections:食品暨應用生物科技學系

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