Ontology highlight
ABSTRACT:
PROVIDER: PRJNA750659 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15367700_1.fastq.gz | Fastqsanger.gz | |||
| SRR15367700_2.fastq.gz | Fastqsanger.gz | |||
| SRR15367701_1.fastq.gz | Fastqsanger.gz | |||
| SRR15367701_2.fastq.gz | Fastqsanger.gz | |||
| SRR15367702_1.fastq.gz | Fastqsanger.gz |
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Project description:F. nucleatum-derived succinic acid induces tumor resistance to immunotherapy in colorectal cancer
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Project description:F. nucleatum-derived succinic acid induces tumor resistance to immunotherapy in colorectal cancer
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Project description:At present, the mechanisms underlying the association between gut microbiota metabolites and immunotherapy in CRC remain unknown. Here, we conducted a multiomics analysis of a cohort of patients with mCRC and found that F.nucleatum was more abundant in patients who did not respond to immunotherapy. We also found that F. nucleatum diminished the sensitivity to anti-PD-1 mAb through its metabolite succinic acid. Accordingly, patients with lower serum succinic acid levels achieved a better response to immunotherapy. Mechanistically, F.nucleatum-derived succinic acid suppressed the cGAS-interferon-β pathway, consequently dampening the antitumor response by limiting CD8+ T-cell trafficking to the tumor microenvironment in vivo. Treatment with metronidazole reduced intestinal F.nucleatum abundance and thereby decreased serum succinic acid levels, thus resensitizing the tumors to immunotherapy in vivo. Collectively, our findings indicate that F. nucleatum and its metabolite succinic acid induce tumor resistance to immunotherapy and offer new insights into microbiota-metabolite-immune crosstalk in CRC.
2023-10-01 | GSE181337 | GEO
Project description:At present, the mechanisms underlying the association between gut microbiota metabolites and immunotherapy in CRC remain unknown. Here, we conducted a multiomics analysis of a cohort of patients with mCRC and found that F.nucleatum was more abundant in patients who did not respond to immunotherapy. We also found that F. nucleatum diminished the sensitivity to anti-PD-1 mAb through its metabolite succinic acid. Accordingly, patients with lower serum succinic acid levels achieved a better response to immunotherapy. Mechanistically, F.nucleatum-derived succinic acid suppressed the cGAS-interferon-β pathway, consequently dampening the antitumor response by limiting CD8+ T-cell trafficking to the tumor microenvironment in vivo. Treatment with metronidazole reduced intestinal F.nucleatum abundance and thereby decreased serum succinic acid levels, thus resensitizing the tumors to immunotherapy in vivo. Collectively, our findings indicate that F. nucleatum and its metabolite succinic acid induce tumor resistance to immunotherapy and offer new insights into microbiota-metabolite-immune crosstalk in CRC.
2023-12-01 | GSE209864 | GEO
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.
2018-11-06 | GSE122182 | GEO
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
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
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.
2022-08-21 | GSE192400 | GEO
Project description:We examined how the immune microenvironment molds tumor evolution in a longitudinal dataset of colorectal cancer liver metastases. Through multiplexed analyses, the immune microenvironment exerts a strong selection pressure during treatment of CLM tumor. Increasing infiltration of T cell were associated with favorable outcomes and sensitive response to chemotherapy ± Bevacizumab. Activation of fatty acid metabolism, xenobiotic metabolism, insulin receptor signaling pathway and neutrophils infiltration were observed in progressive tumors. TCR diversity in response metastatic regions was significantly increased compared with non-responder. Bevacizumab containing regimen facilitated T cell infiltrating to the tumor microenvironment which might consequently benefit from checkpoint immunotherapy. In responding patients, mutation load from plasma were reduced from baseline, but changed slightly in tumor tissues. This integrative and comparative omics analysis provides a new paradigm for understanding the evolution and treatment resistance of colorectal cancer liver metastases, with implications for identifying ways to advance treatment regimen and monitoring treatment response of colorectal cancer liver metastases.
2020-03-08 | GSE136114 | GEO
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.
2017-07-28 | GSE90944 | GEO