ArticleToxicology and applied pharmacology2016
SATB2 expression increased anchorage-independent growth and cell migration in human bronchial epithelial cells.
Article in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Loss of MEG3 promotes migration and invasion of nickel-transformed cells, partially via upregulation of RUNX2.Toxicology and applied pharmacology · 2026Article
- SATB2 dysregulation generates a novel circular RNA and drives KRAS-like transcriptional reprogramming and transformation-associated phenotypes.Cell communication and signaling : CCS · 2026Article
- Review
- SATB2 induction of a neural crest mesenchyme-like program drives melanoma invasion and drug resistance.eLife · 2021Article
- Wrong place, wrong time: Runt-related transcription factor 2/SATB2 pathway in bone development and carcinogenesis.Journal of carcinogenesis · 2021Review
- SATB2 is a novel biomarker and therapeutic target for cancer.Journal of cellular and molecular medicine · 2020Review
- Deregulation of SATB2 in carcinogenesis with emphasis on miRNA-mediated control.Carcinogenesis · 2019Review
- Role of miR-31 and SATB2 in arsenic-induced malignant BEAS-2B cell transformation.Molecular carcinogenesis · 2018Article
- Oncogenic and tumor suppressive roles of special AT-rich sequence-binding protein.Journal of carcinogenesis · 2018Review
- Molecular Mechanisms of Malignant Transformation by Low Dose Cadmium in Normal Human Bronchial Epithelial Cells.PloS one · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.