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Intracellular Fusobacterium nucleatum infection increases METTL3-mediated m6A methylation to promote the metastasis of esophageal squamous cell carcinoma

ABSTRACT: In order to examine the alterations of m6A modifications in particular genes during Fn infection, we conducted differential transcriptome sequencing and differential m6A-sequencing with the aim of analyzing the alterations in expression and map the m6A modification in Fn-infected Eca109 cell and control Eca109 cell.

ORGANISM(S): Homo sapiens

PROVIDER: GSE240349 | GEO | 2025/09/01

REPOSITORIES: GEO

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Intracellular Fusobacterium nucleatum infection increases METTL3-mediated m6A methylation to promote the metastasis of esophageal squamous cell carcinoma.

Project description:IntroductionThe tumor-associated microbiota plays a vital role in cancer development. Accumulating evidence shows that Fusobacterium nucleatum (Fn) participates in the progression of multiple tumor types. However, the underlying mechanisms remain unclear.ObjectivesThis study examined the expression of methyltransferase-like protein 3 (METTL3) during Fn infection and elucidated the function and pathway of Fn-induced m6A methylation in esophageal squamous cell carcinoma (ESCC).MethodsThe abundance of Fn in patient tissues was determined by qPCR. Western blot, qRT-PCR, and immunohistochemistry were performed to measure METTL3 expression in cells and tissues. METTL3 function was evaluated in vitro by colony formation and cell migration assays. MeRIP-qPCR was performed to determine the relationship between METTL3 and c-Myc. In addition, the half-lives of genes that are downstream of METTL3 were determined with RNA stability assays.ResultsFn was enriched in hepatocellular carcinoma (HCC), breast cancer (BRCA), ESCC, and colorectal cancer (CRC) tumor tissues. METTL3 expression was positively associated with Fn abundance in ESCC tissues. Fn could survive and proliferation as well as increase METTL3 expression in ESCC, HCC, CRC, and BRCA cells. Moreover, METTL3 overexpression promoted ESCC cells proliferation, migration in vivo and in vitro. Mechanistically, Intracellular Fn infection increases METTL3 transcription. METTL3 promoted c-Myc mRNA methylation in the 3'-untranslated Region (3'-UTR) and enhanced its mRNA stability in a YTH N6-Methyladenosine RNA binding protein 1(YTHDF1)-dependent manner, which contributes to Fn induced ESCC proliferation and metastasis.ConclusionsThis study indicates that intracellular Fn infection promotes ESCC development and metastasis, and eradicating Fn infection may be a promising strategy for treating ESCC.

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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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RNA-seq of human iNKT cell lines primed with aGalCer vs Fusobacterium nucleatum

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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.

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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.

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Fusobacterium nucleatum-driven mitophagy facilitates endosymbiosis in macrophages and promotes esophageal squamous cell carcinoma metastasis

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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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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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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.

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