Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 30-36 |
| Number of pages | 7 |
| Journal | Toxicology and Applied Pharmacology |
| Volume | 293 |
| DOIs | |
| State | Published - Feb 15 2016 |
| Externally published | Yes |
Bibliographical note
Funding Information:This study was supported by National Institutes of Health grant RO1 ES022935 , ES023174 and National Institute of Environmental Health Sciences grant P30ES000260 .
Publisher Copyright:
© 2016 Elsevier Inc.
Keywords
- Cell migration
- Metal carcinogenesis
- SATB2
