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Effect of Fusobacterium nucleatum (Fn) infection or Fn-Dps treatment on gene expression of esophageal carcinoma Kyse150 and Kyse30 cells

ABSTRACT: Effect of Fusobacterium nucleatum (Fn) infection or Fn-Dps treatment on gene expression of esophageal carcinoma Kyse150 and Kyse30 cells

PROVIDER: PRJNA924024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23085121_1.fastq.gz	Fastqsanger.gz
	SRR23085121_2.fastq.gz	Fastqsanger.gz
	SRR23085122_1.fastq.gz	Fastqsanger.gz
	SRR23085122_2.fastq.gz	Fastqsanger.gz
	SRR23085123_1.fastq.gz	Fastqsanger.gz

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Effect of Fusobacterium nucleatum (Fn) infection or Fn-Dps treatment on gene expression of esophageal carcinoma Kyse150 and Kyse30 cells

Project description:Kyse150 and Kyse30 cells were infected by Fn (the MOI of 1:10) or treated with Fn-Dps (1 μM) for 48 h

2023-06-01 | GSE222917 | GEO

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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The Fusobacterium Nucleatum (Fn) in colorectal carcinogenesis

Project description:The Fusobacterium Nucleatum (Fn) in colorectal carcinogenesis

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Gastric cancer cells treated with exosomes derived from Fusobacterium nucleatum infected MKN-28 cells [RNA-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 RNA-seq data for gene expression profiling.

2023-06-07 | GSE214817 | GEO

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

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Phagocytes as Trojan horse for Fusobacterium nucleatum routing to the tumor tissues and enhance tumor metastasis

Project description:The facultative intracellular bacterium Fusobacterium nucleatum (Fn), mediates tumorigenesis and progression in CRC. However, the origin of intracellular Fn and the role of Fn-infected phagocytes in tumor microenvironment remains unclear. Here, we observed Fn-infected neutrophils/macrophages (PMNs/MΦ) is accumulated in CRC tumor tissues. Fn can survive inside of PMNs by reducing intracellular ROS levels. The lysozyme inhibitor Fn-MliC induced the expression of the CX3CR1 which suppressed apoptosis of phagocytes. Fn-infected phagocytes can transfer Fn to tumor cells, and Fn-infected CRC cells recruited PMNs and MΦ/monocytes through the CXCL2/8-CXCR2 and CCL5/CCR5 axis. Intracellular Fn upregulated PD-L1 expression through activating NF-κB/STAT3 pathway in PMNs. PD-L1+ PMNs infiltration promotes CRC metastasis and weaken the efficacy of immunotherapy, and eradication intracellular Fn infection retarded the Fn promoted tumor progressing in mice. These results suggest that Fn volved efficient strategies to exploit phagocytes to home to tumor tissues, inhibited immune responses and facilitate tumor metastasis.

2024-01-01 | GSE243383 | GEO

Fn-Dps, a novel virulence factor of Fusobacterium nucleatum, disrupts erythrocytes and promotes metastasis in colorectal cancer.

Project description:Fusobacterium nucleatum (Fn) is a critical colorectal cancer (CRC)-associated bacterium. DNA hunger/stationary phase protective proteins (Dps) are bacterial ferritins that protect DNA from oxidative stress. However, little is known about the regulatory roles of Fn-Dps towards host cellular functions. Here, we identified Fn-Dps from the culture supernatant of Fn by mass spectrometry, and prepared the recombinant of Fn-Dps protein. We show a novel virulence protein of Fn, Fn-Dps, which lyses and disrupts erythrocytes by the competition for iron acquisition. Also, Fn-Dps facilitates intracellular survival of Fn in macrophages by upregulating the expression of the chemokine CCL2/CCL7. In addition, Fn-Dps can elicit a strong humoral immune response, and mucosal immunization with Fn-Dps conferred protection against Fn in the intestinal tract. Moreover, a high level of anti-Fn-Dps antibody was prevalent in populations, and elevated anti-Fn-Dps antibody levels were observed in CRC patients. Furthermore, Fn-Dps promotes the migration of CRC cells via the CCL2/CCL7-induced epithelial-mesenchymal transition (EMT) and promotes CRC metastasis in vivo.

| S-EPMC9873182 | biostudies-literature

ESCC KYSE150 cells: TPA treatment vs. control

Project description:Complete lncRNA and mRNA expression profile of ESCC KYSE150 cells and TPA-treatment KYSE150 cells

2024-02-01 | GSE167247 | GEO

Fn multispecies biofilm experiment

Project description:This study was conducted to identify whether F. nucleatum has species or group specific transcriptional responses by analyzing dual species biofilms containing either early or late colonizers and utilizing microarrays to identify altered gene expression of F. nucleatum.

2011-11-30 | E-MEXP-3058 | biostudies-arrayexpress

Fusobacterium nucleatum Induces PD-L1 Expression by Tumor-Associated Macrophages and Inhibits Anti-Tumor Immunity in Colorectal Cancer.

Project description:Fusobacterium nucleatum (Fn) infection has been linked to the initiation and development of colorectal cancer (CRC). However, the underlying mechanisms remains unexplored. Tissues from Fn-infected mice were first collected for single-cell RNA sequencing. we investigated the correlation between Fn infection and accumulations of tumor associated macrophages (TAMs) in tissues from human CRC or AOM/DSS treated mice. The impact of Fn on biological function of TAMs were interrogated. We deciphered the mechanisms for interaction between Fn and TAMs in CRC. We explored the impact of Fn infection on immune-checkpoint blockade (ICB) treatment in a multicohort study.The analysis of single-cell RNA sequencing revealed an enrichment of TAMs in Fn positive tissues. A significant correlation between Fn DNA level and TAMs was observed. Functionally, Fn could recruit TAMs in CRC tissues and promote their biological functions by enhancing PD-L1 expression and thus suppressing CD8+ T cells. Mechanistically, Fn infection led to increased secreted IL-6 via TLR4/MyD88/NF-κB pathways, and the activated IL-6/STAT3 pathway enhanced PD-L1 expression in TAMs. By using several mice models, we found IL-6 inhibition, loss of MyD88 or anti-PD-L1 treatment could significantly inhibit tumorigenesis. Clinically, Fn positive patients tended to be more sensitive to ICB treatment, with a better prognosis than Fn-negative patients.

2022-08-18 | GSE211257 | GEO

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