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ABSTRACT: Fusobacterium nucleatum-gastric cancer cell line co-culture

PROVIDER: PRJNA630089 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11671440.fastq.gz	Fastqsanger.gz
	SRR11671441.fastq.gz	Fastqsanger.gz
	SRR11671442.fastq.gz	Fastqsanger.gz
	SRR11671443.fastq.gz	Fastqsanger.gz
	SRR11671444.fastq.gz	Fastqsanger.gz

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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.

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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.

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