Wu Feng, Jordan Ashley, Kluz Thomas, Shen Steven, Sun Hong, Cartularo Laura A, Costa Max
Department of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA.
Center for Health Informatics and Bioinformatics, New York University Langone Medical Center, New York, NY 10016, USA.
Toxicol Appl Pharmacol. 2016 Feb 15;293:30-6. doi: 10.1016/j.taap.2016.01.008. Epub 2016 Jan 11.
The special AT-rich sequence-binding protein 2 (SATB2) is a protein that binds to the nuclear matrix attachment region of the cell and regulates gene expression by altering chromatin structure. In our previous study, we reported that SATB2 gene expression was induced in human bronchial epithelial BEAS-2B cells transformed by arsenic, chromium, nickel and vanadium. In this study, we show that ectopic expression of SATB2 in the normal human bronchial epithelial cell-line BEAS-2B increased anchorage-independent growth and cell migration, meanwhile, shRNA-mediated knockdown of SATB2 significantly decreased anchorage-independent growth in Ni transformed BEAS-2B cells. RNA sequencing analyses of SATB2 regulated genes revealed the enrichment of those involved in cytoskeleton, cell adhesion and cell-movement pathways. Our evidence supports the hypothesis that SATB2 plays an important role in BEAS-2B cell transformation.
富含AT序列结合蛋白2（SATB2）是一种与细胞的核基质附着区域结合并通过改变染色质结构来调节基因表达的蛋白质。在我们之前的研究中，我们报道了在被砷、铬、镍和钒转化的人支气管上皮BEAS-2B细胞中诱导了SATB2基因表达。在本研究中，我们表明在正常人支气管上皮细胞系BEAS-2B中SATB2的异位表达增加了非锚定依赖性生长和细胞迁移，同时，shRNA介导的SATB2敲低显著降低了镍转化的BEAS-2B细胞中的非锚定依赖性生长。对SATB2调控基因的RNA测序分析揭示了参与细胞骨架、细胞粘附和细胞运动途径的基因的富集。我们的证据支持SATB2在BEAS-2B细胞转化中起重要作用这一假说。
