title: Chronic inflammation confers to the metabolic reprogramming associated with tumorigenesis of colorectal cancer.
abstract: It's well known that microenvironment inflammatory signals could promote cancer development and progression. In colorectal cancer (CRC), chronic inflammation is a major driving mechanism for the development of CRC in patients having long-standing inflammatory bowel disease (IBD). Though it has been addressed that cancer cells ferment much of their glucose supply into lactate regardless of the presence of oxygen, it is unclear whether cell metabolism has been reprogramed during the process from IBD to CRC. Herein, with dextran sulfate sodium (DSS)-induced mouse colitis model, we found that inflammation upregulated key glycolytic enzymes expression via activation of STAT3/c-Myc signaling pathway. Interestingly, during the whole phase of chronic inflammation, the key metabolic enzymes demonstrated increased expression constantly, indicating the metabolic reprogramming was induced by long-term inflammatory signal. Moreover, either the inhibition of STAT3 signaling or c-Myc activity could block the glycolytic enzymes expression induced by interleukin 6 (IL-6). Thus, we presented the view that inflammation could induce the metabolic reprogramming and promote the progression from chronic colitis to colorectal cancer.
authors.affiliation: a The State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology , The Fourth Military Medical University , Xian , China.
authors.forename: Dingding
authors.initials: D
authors.lastname: Qu
authors.affiliation: a The State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology , The Fourth Military Medical University , Xian , China.
authors.forename: Liangliang
authors.initials: L
authors.lastname: Shen
authors.affiliation: b State Key Laboratory of Cancer Biology , Xijing Hospital of Digestive Diease, Xijing Hospital, The Fourth Military Medical University , Xian , China.
authors.forename: Shaoqing
authors.initials: S
authors.lastname: Liu
authors.affiliation: a The State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology , The Fourth Military Medical University , Xian , China.
authors.forename: Huichen
authors.initials: H
authors.lastname: Li
authors.affiliation: a The State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology , The Fourth Military Medical University , Xian , China.
authors.forename: Yongzheng
authors.initials: Y
authors.lastname: Ma
authors.affiliation: b State Key Laboratory of Cancer Biology , Xijing Hospital of Digestive Diease, Xijing Hospital, The Fourth Military Medical University , Xian , China.
authors.forename: Ruohan
authors.initials: R
authors.lastname: Zhang
authors.affiliation: b State Key Laboratory of Cancer Biology , Xijing Hospital of Digestive Diease, Xijing Hospital, The Fourth Military Medical University , Xian , China.
authors.forename: Kaichun
authors.initials: K
authors.lastname: Wu
authors.affiliation: a The State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology , The Fourth Military Medical University , Xian , China.
authors.forename: Libo
authors.initials: L
authors.lastname: Yao
authors.affiliation: b State Key Laboratory of Cancer Biology , Xijing Hospital of Digestive Diease, Xijing Hospital, The Fourth Military Medical University , Xian , China.
authors.forename: Jipeng
authors.initials: J
authors.lastname: Li
authors.affiliation: a The State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology , The Fourth Military Medical University , Xian , China.
authors.forename: Jian
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D063646:Carcinogenesis / Q000473:pathology*; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D002908:Chronic Disease; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000473:pathology*; D003106:Colon / Q000473:pathology; D015179:Colorectal Neoplasms / Q000473:pathology*; D016264:Dextran Sulfate / Q000633:toxicity; D004195:Disease Models, Animal; D006019:Glycolysis; D006801:Humans; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D059016:Tumor Microenvironment
chemical_list: D015850:Interleukin-6; C489428:Myc protein, mouse; D016271:Proto-Oncogene Proteins c-myc; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; C577686:interleukin-6, mouse; D016264:Dextran Sulfate
keywords: Chronic inflammation; IL-6; STAT3; c-Myc; metabolic reprogramming