title: PPARα Promotes Cancer Cell Glut1 Transcription Repression.
abstract: Abundant nutrient availability including glucose and amino acids plays an important role in maintaining cancer cell energetic and biosynthetic pathways. As a nuclear receptor, peroxisome-proliferator-activated receptor α (PPARα) regulates inflammation and cancer progression, however, it is still unclear the interaction of PPARα with the cancer cell glucose metabolism. Here we found that PPARα reduced Glut1 (Glucose transporter 1) protein and gene levels in HCT-116, SW480, HeLa, and MCF-7 cancer cell lines. In contrast, silenced PPARα reversed this event. Further analysis shows that PPARα directly targeted the consensus PPRE motif of Glut1 promoter region resulting in Glut1 transcription repression. PPARα-mediated Glut1 transcription repression led to decreased influx of glucose in cancer cells. These findings revealed a novel mechanism of PPARα-mediated cancer cell Glut1 transcription repression. J. Cell. Biochem. 118: 1556-1562, 2017. © 2016 Wiley Periodicals, Inc.
authors.affiliation: Department of Oncology, The Affiliated Wujin People's Hospital, Jiangsu University, Changzhou 213162, Jiangsu Province, People's Republic of China.|Institute of Life Science, Jiangsu University, Zhenjiang 212000, Jiangsu Province, People's Republic of China.
authors.forename: Mengli
authors.initials: M
authors.lastname: You
authors.affiliation: Department of Oncology, The Affiliated Wujin People's Hospital, Jiangsu University, Changzhou 213162, Jiangsu Province, People's Republic of China.
authors.forename: Jianhua
authors.initials: J
authors.lastname: Jin
authors.affiliation: Department of Oncology, The Affiliated Wujin People's Hospital, Jiangsu University, Changzhou 213162, Jiangsu Province, People's Republic of China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Liu
authors.affiliation: Institute of Life Science, Jiangsu University, Zhenjiang 212000, Jiangsu Province, People's Republic of China.
authors.forename: QingGang
authors.initials: Q
authors.lastname: Xu
authors.affiliation: Institute of Life Science, Jiangsu University, Zhenjiang 212000, Jiangsu Province, People's Republic of China.
authors.forename: Juanjuan
authors.initials: J
authors.lastname: Shi
authors.affiliation: Department of Oncology, The Affiliated Wujin People's Hospital, Jiangsu University, Changzhou 213162, Jiangsu Province, People's Republic of China.|Institute of Life Science, Jiangsu University, Zhenjiang 212000, Jiangsu Province, People's Republic of China.
authors.forename: Yongzhong
authors.initials: Y
authors.lastname: Hou
mesh_terms: D045744:Cell Line, Tumor; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D005947:Glucose / Q000378:metabolism; D051272:Glucose Transporter Type 1 / Q000235:genetics* / Q000378:metabolism; D045325:HCT116 Cells; D006367:HeLa Cells; D006801:Humans; D061986:MCF-7 Cells; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism*; D047493:PPAR alpha / Q000378:metabolism*; D011401:Promoter Regions, Genetic
chemical_list: D051272:Glucose Transporter Type 1; D047493:PPAR alpha; C495677:SLC2A1 protein, human; D005947:Glucose
keywords: CELL SIGNALING; GLUT1; PPARα; TRANSCRIPTION REPRESSION