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SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior

ABSTRACT: SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior

PROVIDER: PRJNA312106 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3169290.fastq.gz	Fastqsanger.gz
	SRR3169300_1.fastq.gz	Fastqsanger.gz
	SRR3169300_2.fastq.gz	Fastqsanger.gz
	SRR3169291.fastq.gz	Fastqsanger.gz
	SRR3169301_1.fastq.gz	Fastqsanger.gz

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SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [ChIP-Seq]

Project description:We report the distribution of human SATB2 in a primary zebrafish melanoma that overexpresses human SATB2, and H3K27Ac histone marks in zebrafish melanomas overexpressing either EGFP (control) or human SATB2.

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SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA-Seq]

Project description:We report gene expression data for zebrafish melanomas overexpressing human SATB2 and EGFP.

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SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior

Project description:This SuperSeries is composed of the SubSeries listed below.

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Danio rerio

Project description:SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [ChIP-Seq]

| PRJNA312108 | ENA

Danio rerio

Project description:SATB2 induces transcriptional programs in melanoma that lead to metastatic behavior [RNA-Seq]

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ChIP-seq for Satb2 in E15 cortex

Project description:The goal of the study was to identify the binding site of SATB2 in wild-ype cortex by performing ChIP-seq using SATB2 antibody. E15 cortical tissues were dissected, lysed and fixed. Chromatin was prepared by sonication. Sequences bound by SATB2 protein was precipitated using a SATB2 antibody. Sequencing was performed on Illumina Genome Analyzer II. SATB2 binding peaks were called using MACS. ChIP for Satb2, followed by sequencing on Illumina Genome Analyzer II platform

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Gene expression signatures of SATB2-defficient vs wild-type adult neocortex

Project description:During CNS development, the nuclear protein SATB2 is expressed in superficial cortical layers and determines projection neuron identity. In the adult CNS, SATB2 is expressed in pyramidal neurons of all cortical layers and is a regulator of synaptic plasticity and long-term memory. Common variation in SATB2 locus confers risk of schizophrenia whereas rare, de novo structural and single nucleotide variants cause severe intellectual disability and absent or limited speech. To which extent symptoms in SATB2-related human pathologies depend on developmental or adult functions of the protein remains to be established. To characterize differences in SATB2 molecular function in developing vs adult neocortex, we compared SATB2 protein interactomes and SATB2-driven gene expression programs at the two ontogenetic stages by co-IP mass spectrometry and RNAseq analyses, respectively. Our results demonstrated that 1) SATB2 interacts with different protein networks at the two ontogenetic stages, with a switch from transcriptional repression towards organization of chromatin structure and 2) SATB2 determines differential transcriptional programs in neonatal vs adult cortex.

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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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Project description:A key step for metastatic outgrowth involves the generation of a deeply altered microenvironment (niche) that supports the malignant behavior of cancer cells. The complexity of the metastatic niche has posed a significant challenge in elucidating the underlying programs driving its origin. Here, by focusing on early stages of breast cancer metastasis to the lung in mice, we describe a cancer-dependent chromatin remodeling and activation of developmental programs in alveolar type 2 (AT2) cells within the niche. We show that metastatic cells can prime AT2 cells into a reprogrammed multilineage state. In turn, this cancer-induced reprogramming of AT2 cells promoted stem-like features in cancer cells and enhanced their initiation capacity. In conclusion, we propose the concept of "reflected stemness" as an early phenomenon during metastatic niche initiation, wherein metastatic cells reprogram the local tissue into a stem-like state that enhances intrinsic cancer-initiating potential, creating a positive feedback loop where tumorigenic programs are amplified.

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