Low glucose transporter SLC2A5-inhibited human normal adjacent lung adenocarcinoma cytoplasmic pro-B cell development mechanism network

Mol Cell Biochem. 2015 Jan;399(1-2):71-6. doi: 10.1007/s11010-014-2233-x. Epub 2014 Oct 18.

Abstract

Solute carrier family 2 (facilitated glucose/fructose transporter) member 5 (SLC2A5)-inhibited seven different molecular Pearson mutual-positive-correlation networks constructed by 24 overlapping molecules from 368 GRNInfer and 34 Pearson under SLC2A5 CC ≤-0.25 in low human normal adjacent tissues were compared with high lung adenocarcinoma. Based on GO, KEGG, GenMAPP, BioCarta, and disease databases, our result showed that low SLC2A5-inhibited network included Golgi apparatus of AP1M2_1; cell cycle of CUL7, SAC3D1; protein amino acid dephosphorylation of STYXL1; pro-B cell-cell differentiation of SOX4_3; and FAD biosynthesis of FLAD1. Thus, we propose low glucose transporter SLC2A5-inhibited human normal adjacent lung adenocarcinoma cytoplasmic pro-B cell development mechanism network through repression of protein amino acid dephosphorylation to FAD biosynthesis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / immunology
  • Adenocarcinoma / metabolism*
  • Adenocarcinoma of Lung
  • B-Lymphocytes / physiology
  • Biosynthetic Pathways
  • Flavin-Adenine Dinucleotide / biosynthesis
  • Gene Expression
  • Glucose Transporter Type 5 / genetics
  • Glucose Transporter Type 5 / metabolism*
  • Humans
  • Lung / metabolism
  • Lung Neoplasms / genetics
  • Lung Neoplasms / immunology
  • Lung Neoplasms / metabolism*

Substances

  • Glucose Transporter Type 5
  • SLC2A5 protein, human
  • Flavin-Adenine Dinucleotide