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ABSTRACT: Fusobacterium nucleatum downregulated MLH1 expression in colorectal cancer by activating autophagy-lysosome pathway

PROVIDER: PRJNA1259493 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33449340.fastq.gz	Fastqsanger.gz
	SRR33449341.fastq.gz	Fastqsanger.gz
	SRR33449342.fastq.gz	Fastqsanger.gz
	SRR33449343.fastq.gz	Fastqsanger.gz
	SRR33449344.fastq.gz	Fastqsanger.gz

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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.

2020-04-20 | GSE144143 | 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.

2021-02-23 | GSE141805 | GEO

SLAM-seq reveals the promotive role of NDRG1 in Fusobacterium nucleatum-induced Tumorigenesis in Colorectal Cancer.

Project description:We report the characterization of transcript dynamics in human colorectal cancer HCT116 cells during Fusobacterium nucleatum infection using thiol-linked alkylation for the metabolic sequencing of RNA (SLAMseq).

2025-05-17 | GSE297086 | GEO

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.

2024-05-13 | GSE267317 | GEO

Gene expression of THP-1 macrophages co-cultured with F. nucleatum under iron-deficient and iron-overload conditions

Project description:Fusobacterium nucleatum (F. nucleatum) contributes to the development of colorectal cancer (CRC) by inducing chronic inflammation. We found that iron deposition in macrophages is associated with poor prognosis of CRC patients with high amount of F. nucleatum. To explore the impact of iron on macrophage properties in the presence of F. nucleatum, we conducted RNA sequencing of THP-1 macrophages pretreated with ferric anmonium citrate (FAC) or deferoxamine (DFO), followed by treatment with F. nucleatum. Several chemokine genes were differentially increased in FAC-treated cells when compared with DFO-treated cells, suggesting that iron is required for the efficient induction of tumor-promoting chemokines in macrophages upon F. nucleatum infection. Our results suggest a prognostic role for iron in F. nucleatum-positive CRC.

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Effect of Fusobacterium nucleatum on human HUVEC cells

Project description:Localization of Fusobacterium nucleatum in the placenta may be associated with pregnancy complications including preeclampsia (PE), but its specific pathobiology is unknown. Our aim was to analyze the effect of Fusobacterium nucleatum on HUVEC cells to further elucidate placental dysfunction in the context of Fusobacterium nucleatum infestation.

2024-06-08 | GSE269085 | GEO

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.

2021-10-19 | GSE173549 | GEO

Fusobacterium nucleatum promotes colorectal cancer cells adhesion to endothelial cells and facilitates extravasation and metastasis by inducing ALPK1/NF-κB/ICAM1 axis

Project description:Fusobacterium nucleatum-treated HCT116 cells reported an increased adhesion to endothelial cells compared with PBS control. To understand the underlying mechanisms of Fusobacterium nucleatum-induced intercellular adhesion ability of CRC cells, we performed RNA-sequencing in HCT116 cells with or without Fusobacterium nucleatum treatment with three independent biological replicates.

2022-03-09 | GSE171611 | GEO

Expression data of miRNA profile from colorectal cancer and the adjacent normal tissues infected with F. nucleatum

Project description:Expression data of miRNA profile from colorectal cancer and the adjacent normal tissues infected with F. nucleatum. Colorectal cancer(CRC) is among the most common cancer types in the world and one of the most lethal cancers. Fusobacterium nucleatum (F. nucleatum) plays an etiologic role in the development of colorectal cancer, but specific tumor molecules involved in the progression of CRC induced by F. nucleatum is not clear. This study investigated some miRNAs and the genes involved in the progression of F. nucleatum-induced colorectal cancer by Affymetrix miRNA microarray technology. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes between Colorectal cancer and the adjacent normal tissues (CONTROL) infected without F. nucleatum . The miRNA array was performed using the affymetrix GeneChip® miRNA 3.0 Array (Affymetrix, Santa Clara, California, United States). The chip was processed using a commercial Affymetrix array service (GeneTech Biotechnology Limited Company, Shanghai, China). The affymetrix GeneChip® miRNA 3.0 Array contains 2,999 probe sets unique to human, mouse and rat pre-miRNA hairpin sequences, 2,216 human snoRNA and scaRNA probe sets and covers 153 organisms (19,724 probe sets). Raw data sets were extracted from all Cel files (raw intensity file) after scanning of slides. These raw data sets were separately analyzed using Expression Console and GeneSpring GX12.5 software followed by differential miRNA expression, fold change & cluster analysis.

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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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