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Homo sapiens

ABSTRACT: RNA-seq in HT-29 colorectal cancer cells after F. nucleatum treatment

PROVIDER: PRJNA356417 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5080871_1.fastq.gz	Fastqsanger.gz
	SRR5080871_2.fastq.gz	Fastqsanger.gz
	SRR5080872_1.fastq.gz	Fastqsanger.gz
	SRR5080872_2.fastq.gz	Fastqsanger.gz
	SRR5080873_1.fastq.gz	Fastqsanger.gz

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RNA-seq in HT-29 colorectal cancer cells after F. nucleatum treatment

Project description:To elucidate whether F. nucleatum plays a role in colorectal cancer tumorigenesis, RNA-seq analysis was performed to compare the gene expression profiles of F. nucleatum treated HT-29 cell line or not.

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Fusobacterium nucleatum upregulates the immune inhibitory receptor PD-L1 in intestinal epithelial cells via the activation of ALPK1

Project description:Fusobacterium nucleatum is a Gram-negative oncobacterium that is associated with colorectal cancer. The molecular mechanisms utilized by F. nucleatum to promote colorectal tumor development have largely focused on adhesin-mediated binding to the tumor tissue and on the pro-inflammatory capacity of F. nucleatum. However, the exact manner in which F. nucleatum promotes inflammation in the tumor microenvironment and subsequent tumor promotion remains underexplored. Here, we show that both live F. nucleatum and sterile F. nucleatum-conditioned medium promote CXCL8 release from the intestinal adenocarcinoma HT-29 cell line. We determined that the pro-inflammatory response was ALPK1-dependent in both HEK293 and HT-29 cells and that the released F. nucleatum molecule had characteristics that match those of the pro-inflammatory ALPK1 ligand ADP-heptose or related heptose phosphates. In addition, not only F. nucleatum but also other Fusobacterium species such as F. varium, F. necrophorum and F. gonidiaformans promoted an ALPK1-dependent pro-inflammatory environment, indicating that ADP-heptose or related heptose phosphates secretion is a conserved feature of the Fusobacterium genus. By performing transcriptional analysis of ADP-heptose stimulated HT-29 cells, we found several inflammatory and cancer-related pathways to be differentially regulated, including DNA mismatch repair genes and the immune inhibitory receptor PD-L1. Finally, we show that stimulation of HT-29 cells with F. nucleatum resulted in an ALPK1-dependent upregulation of PD-L1. These results aid in our understanding of the mechanisms by which F. nucleatum can affect tumor development and therapy and pave the way for future therapeutic approaches.

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Project description:Aberrant expression of SOX9 in human colorectal cancer cells suggests its roles in the development of colorectal cancer. To gain insight into SOX9-mediated transcriptional regulation in colorectal cancer cells, we attempted to identify its physiological targets on a genome-scale using chromatin immunoprecipitation (ChIP) followed by sequencing (ChIP-seq) in HT-29, human colorectal cancer cells. SOX9 CHIP-seq was carried out using HT-29 cells.

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Homo sapiens

Project description:Expression data of colorectal cancer HT-29 cells

| PRJNA390254 | ENA

Genome-wide maps of SOX9 binding sites in human colorectal cancer cells

2015-06-08 | GSE63629 | GEO

Expression data of colorectal cancer HT-29 cells

Project description:Colorectal cancer HT-29 cell line is a comonly-used human cancer cell line. We have used this cell line for examining the effect of various anticancer compounds on gene expression and we obtained gene expression data of untreated HT-29 cells as a control data for the analysis.

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RNA-seq of murine breast cancer cell line AT3 infected with F. nucleatum

Project description:Fusobacterium nucleatum (F. nucleatum) is implicated to exacerbate colorectal cancer. However, there is also evidence that the bacterium accumulates on other cancer types such as breast cancer. In order to better understand the transcriptional response of breast cancer cells to infection with F. nucleatum, we performed RNA-seq of the murine breast cancer cell AT3 with F. nucleatum.

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Project description:MIEN1 has been described as a key actor in colorectal cancer (CRC) biogenesis. We have used CRISPR/Cas9 technique to delete the promoter region of MIEN1 in HT-29 CRC cells. RNA-seq experiments revealed that several biological processes related to migration/metastasis were enriched by differentially expressed genes. Genetically modified cells shown decreased migration capacity.

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