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Stable overexpression of IRF8 in hepatocellular carcinoma cells hepa1-6 xenograft derived tumors in C57bl/6 mice

ABSTRACT: Stable overexpression of IRF8 in hepatocellular carcinoma cells hepa1-6 xenograft derived tumors in C57bl/6 mice

PROVIDER: PRJNA700621 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13652126_1.fastq.gz	Fastqsanger.gz
	SRR13652126_2.fastq.gz	Fastqsanger.gz
	SRR13652127_1.fastq.gz	Fastqsanger.gz
	SRR13652127_2.fastq.gz	Fastqsanger.gz

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Stable overexpression of IRF8 in hepatocellular carcinoma cells hepa1-6 xenograft derived tumors in C57bl/6 mice

Project description:Interferon regulatory factor 8 (IRF8), also known as interferon consensus sequence-binding protein, is an essential lineage-specific transcriptional regulator in the IRF family, controls diverse cellular processes and is has been implicated in innate immunity, immune cell differentiation. IRF8 has been shown to have both oncogenic and tumor suppressor activities, in myeloid cells and nonhematopoietic cells. As a transcription factor, other functions which may contribute to its oncogenic and anti tumor potential are not clear. So it is meaningful to study the role of IRF8 in different diseases. The roles and the underlying mechanisms of intrahepatic IRF8 in Hepatocellular carcinoma have not been reported up to date.

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Stable overexpression of IRF8 in hepatocellular carcinoma cells

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Expression changes in Setdb1-knockdown with shRNA in Hepa1-6 cells, a mouse hepatocellular carcinoma line

Project description:SETDB1 is an epigenetic regulator via H3K9me3. Much is not known about the role of SETDB1 in hepatocellular carcinoma. In this study, we established an shRNA-based Setdb1-knockdown strain in the mouse hepatocellular carcinoma line Hepa1-6 and performed RNA sequencing to identify genes regulated by Setdb1.

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Microarray analysis of LRRC3B stable cell derived xenograft tumors

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Next Generation Sequencing Facilitates Quantitative Analysis of Hepa1-6 cells treated with 50 μM TMAO and 50ng/ml TNF-α Transcriptomes

Project description:Liver cancer has a high mortality rate. Chronic inflammation is one of the leading causes of hepatocellular carcinoma. Recent studies suggested high levels of trimethylamine N-oxide (TMAO) may correlate with increased risk of inflammatory-induced liver cancer. However, the mechanisms by which TMAO promotes liver cancer remain elusive. Here, we established a model of inflammatory-induced liver cancer by treating Hepa1-6 cells with TNF-α. TMAO synergistically increased the proliferation, migration and invasion of Hepa1-6 cells in the presence of TNF-α. We conducted bulk RNA-Seq of the TMAO-treated cell model of inflammatory Hepatocellular carcinoma (HCC)

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Stable knockdown of PLAGL2 in hepatocellular carcinoma cells

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Project description:Purpose: investigating paracrine effects of mono- and/or co-cultured LSEC and Hepa1-6 Method: mRNA profiles of mono- and co-cultured LSEC and Hepa1-6 were generated by deep sequencing. Results: The RNA-seq data confirmed that extracellular matrix-encoding genes were up-regulated by co-cultured LSEC with Hepa1-6.

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miRNA Expression in 4 mouse Hepatocellular Carcinoma cells with different lymphatic metastasis potentials

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Gene expression profiles of Hepa1-6 tumors in C57Bl/6 mice

Project description:Chronological change of gene expression profile of Hepa1-6 tumors in C57Bl/6 Two-condition experiment

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