Mao Liang-Chi, Wang Hsi-Ming, Lin You-Yu, Chang Te-Kau, Hsin Yi-Hong, Chueh Pin Ju
Institute of Biomedical Sciences, National Chung Hsing University, Taichung 40227, Taiwan, ROC.
FEBS Lett. 2008 Oct 15;582(23-24):3445-50. doi: 10.1016/j.febslet.2008.09.008. Epub 2008 Sep 18.
Tumor-associated NADH oxidase (tNOX) is a growth-related protein expressed in transformed cells. tNOX knockdown using RNA interference leads to a significant reduction in HeLa cell proliferation and migration, indicating an important role for tNOX in growth regulation and the cancer phenotype. Here, we show that tNOX is down-regulated during apoptosis in HCT116 cells. Treatment with diverse stresses induced a dose- and time-dependent decrease in tNOX expression that was concurrent with apoptosis. Moreover, shRNA-mediated tNOX knockdown rendered cells susceptible to apoptosis, whereas re-expression of tNOX partially recovered cell proliferation. Our results indicate that tNOX is suppressed during apoptosis and demonstrate that tNOX down-regulation sensitizes cells to stress-induced growth reduction, suggesting that tNOX is required for transformed cell growth.
肿瘤相关NADH氧化酶（tNOX）是一种在转化细胞中表达的与生长相关的蛋白质。使用RNA干扰敲低tNOX会导致HeLa细胞增殖和迁移显著减少，表明tNOX在生长调节和癌症表型中起重要作用。在此，我们表明tNOX在HCT116细胞凋亡过程中表达下调。用多种应激处理诱导tNOX表达呈剂量和时间依赖性降低，这与细胞凋亡同时发生。此外，shRNA介导的tNOX敲低使细胞易发生凋亡，而tNOX的重新表达部分恢复了细胞增殖。我们的结果表明tNOX在凋亡过程中受到抑制，并证明tNOX下调使细胞对应激诱导的生长抑制敏感，提示tNOX是转化细胞生长所必需的。
