{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Udayasuryan B"],"funding":["NCI NIH HHS"],"pagination":["eabn4948"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9732933"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(756)"],"pubmed_abstract":["The tumor microbiome is increasingly implicated in cancer progression and resistance to chemotherapy. In pancreatic ductal adenocarcinoma (PDAC), high intratumoral loads of <i>Fusobacterium nucleatum</i> correlate with shorter survival in patients. Here, we investigated the potential mechanisms underlying this association. We found that <i>F. nucleatum</i> infection induced both normal pancreatic epithelial cells and PDAC cells to secrete increased amounts of the cytokines GM-CSF, CXCL1, IL-8, and MIP-3α. These cytokines increased proliferation, migration, and invasive cell motility in both infected and noninfected PDAC cells but not in noncancerous pancreatic epithelial cells, suggesting autocrine and paracrine signaling to PDAC cells. This phenomenon occurred in response to <i>Fusobacter"],"journal":["Science signaling"],"pubmed_title":["<i>Fusobacterium nucleatum</i> induces proliferation and migration in pancreatic cancer cells through host autocrine and paracrine signaling."],"pmcid":["PMC9732933"],"funding_grant_id":["R21 CA238630"],"pubmed_authors":["Umana A","Udayasuryan B","Slade DJ","Verbridge SS","Nguyen TTD","Jones SD","Ahmad RN","Monet Roberts L","Sobol P","Munson JM"],"additional_accession":[]},"is_claimable":false,"name":"<i>Fusobacterium nucleatum</i> induces proliferation and migration in pancreatic cancer cells through host autocrine and paracrine signaling.","description":"The tumor microbiome is increasingly implicated in cancer progression and resistance to chemotherapy. In pancreatic ductal adenocarcinoma (PDAC), high intratumoral loads of <i>Fusobacterium nucleatum</i> correlate with shorter survival in patients. Here, we investigated the potential mechanisms underlying this association. We found that <i>F. nucleatum</i> infection induced both normal pancreatic epithelial cells and PDAC cells to secrete increased amounts of the cytokines GM-CSF, CXCL1, IL-8, and MIP-3α. These cytokines increased proliferation, migration, and invasive cell motility in both infected and noninfected PDAC cells but not in noncancerous pancreatic epithelial cells, suggesting autocrine and paracrine signaling to PDAC cells. This phenomenon occurred in response to <i>Fusobacter","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-04T07:11:07.717Z","creation":"2025-04-04T07:11:07.717Z"},"accession":"S-EPMC9732933","cross_references":{"pubmed":["36256708"],"doi":["10.1126/scisignal.abn4948"]}}