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Tex10 in primordial gem cell-like cell (PGCLC) specification and spermatogenesis

ABSTRACT: Tex10 in primordial gem cell-like cell (PGCLC) specification and spermatogenesis

PROVIDER: PRJNA749589 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15242600_1.fastq.gz	Fastqsanger.gz
	SRR15242600_2.fastq.gz	Fastqsanger.gz
	SRR15242601_1.fastq.gz	Fastqsanger.gz
	SRR15242601_2.fastq.gz	Fastqsanger.gz
	SRR15242602_1.fastq.gz	Fastqsanger.gz

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Tex10 in primordial gem cell-like cell (PGCLC) specification and spermatogenesis

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Project description:GEM-CESAR

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Genome-wide maps of Tex10 and chromatin state in Day 2 primordial germ cell-like cells (PGCLCs)

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RNAi Screening Identifies that TEX10 Promotes the Proliferation of Colorectal Cancer Cells by Increasing NF-κB Activation

Project description:Colorectal cancer (CRC) has become a predominant cancer worldwide. In order to understand the process of carcinogenesis, an shRNA library screening is employed for searching candidate genes that promote proliferation in the CRC cell line HT29. The candidate genes overlapped with differentially expressed genes in 32 CRC tumor tissues in the GEO dataset GSE8671. The seventh-ranked TEX10 is upregulated in CRC and its knockdown decreased cell proliferation. The TEX10 high-expression group exhibits worse overall survival (P = 0.003) and progression-free survival (P < 0.001) than the TEX10 low-expression group. TEX10 depletion decreases the growth of CRC cells in vitro and in vivo. GSEA indicates that the NF-κB pathway is significantly enriched in the genes downregulated by TEX10 knockdown. Mechanistically, TEX10 interacts with p65 and increases its nuclear localization. TEX10 promotes p65 occupancy at gene promoters and regulates the expression of a subset of p65-targeted genes including TNFAIP8, SAT1 and IL6ST. Taken together, this study identifies that TEX10 promotes the proliferation of CRC cells in a p65-dependent manner. In addition, high TEX10 expression is associated with poor prognosis in CRC patients.

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Gene expression of VPA and GEM

Project description:Background: Histone deacetylase (HDAC) is strongly associated with epigenetic regulation and carcinogenesis, and its inhibitors induce the differentiation or apoptosis of cancer cells. Valproic acid (VPA) is one of the clinically available HDAC inhibitors. We investigated the anticancer effects of VPA in combination with gemcitabine (GEM) in cholangiocarcinoma cell line, and explored the mechanisms of the anticancer effects using microarray analysis. Methods: A human cholangiocarcinoma cell line (HuCCT1) was used. The anticancer effects of VPA, or gemcitabine (GEM), and the effects of VPA combined with GEM, were studied by cell proliferation assay. The microarray analysis was performed, the genes were picked up using Gene Spring GX11.5, Ingenuity Pathways Analysis (IPA) was performed, and then the gene-expression was determined by RT-PCR. Results: GEM (5nM) and VPA (0.5mM) reduced by 23%, which significantly augmented the anticancer effect of GEM alone or VPA alone (P<0.01). Using the microarray analysis, forty-three genes were identified with the comparison between GEM group and GEM plus VPA combination group. The interactions were shown between genes of the “Cellular Development” relevant to the differentiation of cancer cell using IPA.

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