Abstract：
GLUT5, a key protein encoded by the SLC2A5 gene, is involved in the uptake of fructose from the intestine. Currently, with the increased consumption of this sugar and the associated increased incidence of obesity, diabetes and cancer, GLUT5 may represent an important molecular target in the prevention and treatment of these diseases. Here, we demonstrate that overexpression of the SNAI1 and SNAI2 transcription factors in cells expressing high levels of SLC2A5 mRNA reduced SLC2A5 gene expression. Furthermore, a histone deacetylase inhibitor, trichostatin A, which induces SNAI1 and SNAI2 expression, inhibits SLC2A5/GLUT5 expression and sensitizes colon cancer cells to cisplatin and oxaliplatin. This finding might have potential relevance for the development of therapeutic treatments aimed at modulating fructose transport or genes involved in this process for use with certain cancers.
摘要：
GLUT5，由SLC2A5基因编码的关键蛋白，参与从肠中摄取果糖。目前,随着这种糖的消费增加和相关的肥胖发病率增加，糖尿病和癌症,GLUT5可能是预防和治疗这些疾病的重要分子靶标。这里,我们证明SNAI1和SNAI2转录因子在表达高水平SLC2A5mRNA的细胞中的过表达降低了SLC2A5基因的表达。此外，组蛋白脱乙酰酶抑制剂，曲古抑菌素A,诱导SNAI1和SNAI2表达，抑制SLC2A5/GLUT5表达并使结肠癌细胞对顺铂和奥沙利铂敏感。这一发现可能与开发旨在调节果糖转运或参与该过程的基因以用于某些癌症的治疗性治疗具有潜在相关性。
