Department of Pathology, School of Medicine, Kyung Hee University, Seoul, Republic of Korea.
FEBS Lett. 2012 Sep 21;586(19):3435-40. doi: 10.1016/j.febslet.2012.07.064. Epub 2012 Jul 28.
Tumor hypoxia may be an indicator of poor survival in cancer patients. Thus, an understanding of the molecular mechanism responsible for hypoxic tumor selection is essential to gain further insight into tumor biology. Our aim in this study was to investigate whether hypoxia-responsive GLTSCR2 contributes to death resistance and increased invasiveness of hypoxia-selected glioblastoma cells. We found that repeated hypoxia downregulates p53-upstream regulator, GLTSCR2, which resulted in increased death resistance and invasive potential of glioblastoma cells. Restoration of GLTSCR2 expression suppressed the malignant potential of hypoxia-selected cells. Our results indicate that GLTSCR2 participates in hypoxia-induced malignant potential.
肿瘤缺氧可能是癌症患者生存不良的一个指标。因此,了解导致肿瘤缺氧选择的分子机制对于深入了解肿瘤生物学至关重要。我们在这项研究中的目的是研究缺氧反应性 GLTSCR2 是否有助于缺氧选择的脑胶质瘤细胞的抗死亡和侵袭能力的增加。我们发现,反复缺氧下调 p53 上游调节因子 GLTSCR2,导致脑胶质瘤细胞的抗死亡能力和侵袭潜能增加。GLTSCR2 表达的恢复抑制了缺氧选择细胞的恶性潜能。我们的结果表明 GLTSCR2 参与了缺氧诱导的恶性潜能。