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The Fusobacterium Nucleatum (Fn) in colorectal carcinogenesis

ABSTRACT: The Fusobacterium Nucleatum (Fn) in colorectal carcinogenesis

PROVIDER: PRJNA594850 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10669494_1.fastq.gz	Fastqsanger.gz
	SRR10669494_2.fastq.gz	Fastqsanger.gz
	SRR10669495_1.fastq.gz	Fastqsanger.gz
	SRR10669495_2.fastq.gz	Fastqsanger.gz
	SRR10669496_1.fastq.gz	Fastqsanger.gz

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The Fusobacterium Nucleatum (Fn) in colorectal carcinogenesis

Project description:To elucidate whether Fusobacterium Nucleatum(Fn) plays a role in colorectal cancer tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of Fn treated HCT116 colorectal cancer cell lines.

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Fusobacterium nucleatum promotes colorectal carcinogenesis via an m6A dependent pathway

Project description:Previous reports have indicated that RNA m6A modification plays an important role in colorectal carcinogenesis. We hypothesized that F. nucleatum promoted colorectal carcinogenesis dependent on RNA m6A alterations. To test this hypothesis, we conducted a RNA-seq analysis in HT29 cells cocultured with F. nucleatum and medium control.

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Fusobacterium nucleatum promotes colorectal carcinogenesis via an m6A dependent pathway

Project description:Fusobacterium nucleatum promotes colorectal carcinogenesis via an m6A dependent pathway

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The adhesin RadD enhances Fusobacterium nucleatum tumor colonization and colorectal carcinogenesis

Project description:Fusobacterium nucleatum can bind to host cells and potentiate intestinal tumorigenesis. Here, we used a genome-wide screen to identify an adhesin, RadD, which facilitates the attachment of F. nucleatum to CRC cells in vitro. RadD directly binds to CD147, a receptor overexpressed on CRC cell surfaces, which initiated a PI3K-AKT-NF-κB-MMP9 cascade, subsequently enhancing tumorigenesis in mice. Clinical specimen analysis showed that elevated radD gene levels in CRC tissues correlated positively with activated oncogenic signaling and poor patient outcomes. Finally, blockade of the interaction between RadD and CD147 in mice effectively impaired F. nucleatum attachment and attenuated F. nucleatum-induced oncogenic response. Together, our study provides insights into an oncogenic mechanism driven by F. nucleatum RadD and suggests that the RadD-CD147 interaction could be a potential therapeutic target for CRC.

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Gene expression analysis of human esophageal cancer cells co-cultured with Fusobacterium nucleatum

Project description:This study analyzed changes in gene expression caused by infection with Fusobacterium nucleatum (Fn) in human esophageal cancer (EC) cells. The hypothesis was that Fn infection affects the activation of the stimulator of interferon genes (STING) signaling pathway and the expression of its downstream genes in EC cells. Results revealed interesting upregulated genes related to the STING signaling pathway in response to Fn infection.

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The adhesin RadD enhances Fusobacterium nucleatum tumor colonization and colorectal carcinogenesis

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Fusobacterium nucleatum promotes colorectal cancer metastasis through miR-1322/CCL20 axis and M2 polarization

Project description:Fusobacterium nucleatum-treated LoVo cells reported an increased promoting CRC metastasis effect compared with PBS control. To understand the underlying mechanisms of Fusobacterium nucleatum-induced metastasis ability of CRC cells, we performed RNA-sequencing in LoVo cells s with or without Fusobacterium nucleatum treatment with three independent biological replicates.

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Gastric cancer cells treated with exosomes derived from Fusobacterium nucleatum infected MKN-28 cells [miRNA-seq]

Project description:To investigate the role of Fusobacterium nucleatum (Fn) in the development of gastric cancer, we extracted exosomes from the culture supernatant of MKN-28 cells treated with Fn or PBS, co-cultured them with AGS cells, and analyzed their miRNA-seq data for gene expression profiling.

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Gastric cancer cells treated with exosomes derived from Fusobacterium nucleatum infected MKN-28 cells [RNA-seq]

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Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness [RIP-Seq]

Project description:To investigate the role of Fusobacterium nucleatum-mediated m6A modification, we performed m6A-sequencing to map the m6A modification in control or Fusobacterium nucleatum-treated HCT116 cells.

2022-02-07 | GSE150308 | GEO

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