You Jingwen, Wang Lin, Huang Juxiang, Jiang Minghu, Chen Qingchun, Wang Yangming, Jiang Zhenfu
Biomedical Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China.
Mol Cell Biochem. 2015 Jan;399(1-2):71-6. doi: 10.1007/s11010-014-2233-x. Epub 2014 Oct 18.
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.
在低人正常邻近组织中，当溶质载体家族2（易化葡萄糖/果糖转运蛋白）成员5（SLC2A5）的相关系数（CC）≤ -0.25时，将通过368个基因调控网络推断（GRNInfer）中的24个重叠分子构建的7个不同分子的Pearson相互正相关网络以及34个Pearson网络与高肺腺癌进行比较。基于基因本体论（GO）、京都基因与基因组百科全书（KEGG）、基因图谱（GenMAPP）、生物通路数据库（BioCarta）和疾病数据库，我们的结果表明，低SLC2A5抑制网络包括AP1M2_1的高尔基体；CUL7、SAC3D1的细胞周期；STYXL1的蛋白质氨基酸去磷酸化；SOX4_3的前B细胞分化；以及FLAD1的黄素腺嘌呤二核苷酸（FAD）生物合成。因此，我们提出低葡萄糖转运蛋白SLC2A5抑制人正常邻近肺腺癌细胞质前B细胞发育机制网络是通过抑制蛋白质氨基酸去磷酸化至FAD生物合成实现的。
