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Induction of human SST and PV neurons by expressing a single transcription factor LHX6

ABSTRACT: Induction of human SST and PV neurons by expressing a single transcription factor LHX6

PROVIDER: PRJNA471715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7172392.fastq.gz	Fastqsanger.gz
	SRR7172393.fastq.gz	Fastqsanger.gz
	SRR7172394.fastq.gz	Fastqsanger.gz
	SRR7172395.fastq.gz	Fastqsanger.gz
	SRR7172396.fastq.gz	Fastqsanger.gz

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Induction of human SST and PV neurons by expressing a single transcription factor LHX6

Project description:To systematically explore the effect of LHX6 on neural development and differentiation, we performed RNA-sequencing (RNA-seq) of hPSC-derived GINs at day 50 in vitro.RNAseq results could also confirm alteration of GINs identity with the overexpression of LHX6.

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Project description:There was a remarkable similarity in the molecular properties of the MGE-GFP+ and ES-GFP+ cells. In particular, genes that are important for medial ganglionic eminence (MGE) and cortical interneurons development are both high in expression in both MGE-Lhx6-GFP+ and ES-Lhx6-GFP+ cells (compared to ES-Lhx6-GFP- cells). To investigate how closely ES cells-derived Lhx6-GFP+ cells resembled authentic Lhx6+ MGE cells, and to define the molecular properties of the Lhx6-GFP+ and Lhx6-GFP- cells from differentiated ES cells, we compared their gene expression profiles. We used FACS to purify GFP+ cells from the E12.5 MGE of Lhx6-GFP transgenic mice. ES-Lhx6-GFP+ cells and ES-Lhx6-GFP- cells (both from D12 EB aggregates) were also isolated by fluorescent activated cell sorting (FACS) and all of the RNA samples were subjected to RNA expression microarray analyses.

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Project description:Epigenetic gene silencing by aberrant DNA methylation leads to loss of key cellular pathways in tumorigenesis. DNA methylation-mediated silenced genes in pancreatic cancer were searched by methyl-CpG targeted transcriptional activation (MeTA) method and LHX6 (LIM homeobox 6), a transcription factor involved in embryogenesis and head development, was selected as one of candidate genes. LHX6 was downregulated in most pancreatic cancer cell lines (83%: 10/12) mainly through promoter hypermethylation and histone deacetylation. Furthermore, LHX6 was also methylated in primary pancreatic cancers in a tumor-specific manner (57%: 16/28). In order to assess the biological significance of LHX6 in pancreatic tumorigenesis, we first performed colony formation assay and found that LHX6 re-expression inhibited colony formation in pancreatic cancer cell lines. Similarly, inducible expression of LHX6 inhibited cell proliferation and migration in LHX6 low-expressing pancreatic cancer cell lines. On the other hand, knockdown of LHX6 accelerated cell proliferation in LHX6 high-expressing pancreatic cancer cell lines. Our present results suggest that epigenetic inactivation of LHX6 plays an important role in pancreatic tumorigenesis by promoting cell proliferation.

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