Furuhata T, Tokino T, Urano T, Nakamura Y
Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo, Japan.
Oncogene. 1996 Nov 7;13(9):1965-70.
We have identified a novel gene inducible by wild-type p53. A significant correlation between expression of this gene and p53 status in cells derived from esophageal cancers indicated that this gene is likely to be specifically regulated in a p53-dependent manner. As the predicted amino acid sequence showed a high degree of homology to the family of glycosyl-phosphatidylinositol (GPI)-anchored membrane proteins, we termed this gene GML (GPI-anchored molecule-like protein). Introduction of GML cDNA suppressed the growth of esophageal cancer cells in culture. A correlation between the presence of GML expression and the sensitivity of esophageal cancer cells to anti-cancer drugs implied that the gene product plays a significant role in the apoptotic pathway or cell-cycle regulation induced by p53 after DNA damage.
我们鉴定出了一种可被野生型p53诱导的新基因。该基因在源自食管癌的细胞中的表达与p53状态之间存在显著相关性,这表明该基因可能以p53依赖的方式受到特异性调控。由于预测的氨基酸序列与糖基磷脂酰肌醇(GPI)锚定膜蛋白家族具有高度同源性,我们将该基因命名为GML(GPI锚定分子样蛋白)。导入GML cDNA可抑制培养的食管癌细胞的生长。GML表达的存在与食管癌细胞对抗癌药物的敏感性之间的相关性表明,该基因产物在DNA损伤后由p53诱导的凋亡途径或细胞周期调控中起重要作用。