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SATB2 expression increased anchorage-independent growth and cell migration in human bronchial epithelial cells

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. We show that ectopic expression of SATB2 in normal human bronchial epithelial cell-line BEAS2B increased anchorage-independent growth and cell migration,RNA sequencing analyses of SATB2 regulated genes revealed the enrichment of those involved in cytoskeleton, cell adhesion and cell-movement pathways.

ORGANISM(S): Homo sapiens

PROVIDER: GSE75652 | GEO | 2016/02/01

SECONDARY ACCESSION(S): PRJNA304982

REPOSITORIES: GEO

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Investigation into SATB2 DNA-binding sites and the effect of SATB2 removal on the transcriptome of skeletal muscle satellite cells

Project description:Induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. In our associated paper, we found that the removal of special AT-rich binding protein 2 (SATB2), a nuclear protein that binds matrix attachment regions, is a key event in initiating myogenic differentiation. This study included ChIP-seq analyses to assess the genetic binding sites of SATB2 prior to differentiation and categorize their respective roles within the cell. Furthermore, transcriptome analyses using RNA-seq was conducted on C2C12 cells treated with control siRNA and siRNA against SATB2 prior to differentiation. This was done to assess the changes in transcript expression following the loss of SATB2.

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SATB2 expression increased anchorage-independent growth and cell migration in human bronchial epithelial cells.

Project description: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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Chromatin reorganization during myoblast differentiation involves the caspase-dependent removal of SATB2 [ChIP-seq]

Project description:Induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. Here, we report that removal of special AT-rich binding protein 2 (SATB2), a nuclear protein known to bind matrix attachment regions, is a key event in initiating myogenic differentiation. Deletion of myoblast SATB2 in vitro initiates chromatin remodeling and accelerates differentiation, while in vivo ablation depletes the muscle progenitor pool. Genome wide analysis indicates that SATB2 binding influences both chromatin loop and sub-TAD domain formation. These chromatin changes are both repressive and inductive, as loss of SATB2 leads to expression of differentiation regulatory factors and inhibition of genes that impair this process. Finally, we noted that the differentiation-specific decline in SATB2 protein is dependent on a caspase 7-mediated cleavage event. Taken together, this study demonstrates that temporal control of SATB2 protein is critical for shaping the chromatin environment and coordinating the myogenic differentiation program

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Chromatin reorganization during myoblast differentiation involves the caspase-dependent removal of SATB2 [Hi-C]

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