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RNA-seq of H1299 overexpressing GFP(control) and SALL4

ABSTRACT: RNA-seq of H1299 overexpressing GFP(control) and SALL4

PROVIDER: PRJNA748768 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15210494_1.fastq.gz	Fastqsanger.gz
	SRR15210494_2.fastq.gz	Fastqsanger.gz
	SRR15210495_1.fastq.gz	Fastqsanger.gz
	SRR15210495_2.fastq.gz	Fastqsanger.gz
	SRR15210496_1.fastq.gz	Fastqsanger.gz

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RNA-seq of H1299 overexpressing GFP(control) and SALL4

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HUES cells: control and overexpressing OCT4

Project description:HUES24 cell line was nucleofected with POU5f1 cDNA to overexpress OCT4; This leads to the formation of mesendodermal cells Short- and Long-scales intra- and inter-chromosomal interactions are linked to gene transcription, but the molecular event underlying these structures and how it affects cell fate decision during embryonic development are poorly understood. One of the first embryonic cell fate decisions (i.e mesendoderm determination) is driven by the POU factor OCT4, acting in concert with the high mobility group genes SOX-2 and SOX-17. Here, we identify novel chromatin remodelling mechanism and enhancer function driven by both OCT4 and SALL4 that mediate cell fate switching. We found that OCT4 alters the higher-order chromatin structure at both Sox-2 and Sox-17 loci. OCT4 titrates out cohesin and switches the Sox-17 enhancer from a locked (within an inter-chromosomal Sox-2 enhancer/CTCF/cohesin loop) to an active (within an intra-chromosomal Sox-17 promoter/enhancer/cohesin loop) state. SALL4 concomitantly mobilizes the polycomb complexes at the Soxs loci. Thus, OCT4/SALL4-driven cohesin-and polycombs-mediated changes in higher order chromatin structure mediate instruction of early cell fate in embryonic cells. ChIP anti-OCT4 on chip. results_v2.xls file description: Enriched binding sites. Mutant means oct4 overexpressing cells , wt GFP nucleofected cells.

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Gene expression data from H1299 cells

Project description:MiR-138 has a variety of biological functions because of its capacity to act on different target genes in various cells and tissues; however, the targets of miR-138 in human non-small cell lung cancer cell line H1299 cannot be determined by bioinformatics alone. Thus, H1299 cells overexpressing miR-138 in H1299 cells were subjected to microarray analysis to analyse the differences of gene expression.

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Project description:Transcription factors are important drivers of cancer but the development of therapeutics against these factors has had limited success. We developed a stringent high-throughput chemical genetic screening platform to identify compounds that target oncogene SALL4 dependency in liver cancer. The platform comprises SALL4 low- and high-expressing endogenous cell lines, and engineered SALL4-low isogenic lines overexpressing SALL4. We identified 4 oxidative phosphorylation (OXPHOS) inhibitors, from screening 21,575 natural product extracts, that selectively reduce SALL4-dependent cell viability. ATP synthase inhibitor Oligomycin suppresses SALL4-expressing cancer in culture and in vivo. When aberrantly overexpressed in cancer, SALL4 binds ~50% of OXPHOS and other mitochondrial genes, upregulating their expression. SALL4 upregulation also functionally increases OXPHOS. Our endogenous/isogenic transcription factor-screening platform reveals a therapeutically actionable OXPHOS vulnerability in SALL4-expressing cancer.

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