{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sheridan M"],"funding":["NIDCR NIH HHS","NIDDK NIH HHS","NCI NIH HHS","National Institutes of Health"],"pagination":["109860"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11108982"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(6)"],"pubmed_abstract":["Mechanisms by which <i>Porphyromonas gingivalis</i> (<i>P. gingivalis</i>) infection enhances oral tumor growth or resistance to cell death remain elusive. Here, we determined that <i>P. gingivalis</i> infection mediates therapeutic resistance via inhibiting lethal mitophagy in cancer cells and tumors. Mechanistically, <i>P. gingivalis</i> targets the LC3B-ceramide complex by associating with LC3B via bacterial major fimbriae (FimA) protein, preventing ceramide-dependent mitophagy in response to various therapeutic agents. Moreover, ceramide-mediated mitophagy is induced by Annexin A2 (ANXA2)-ceramide association involving the E142 residue of ANXA2. Inhibition of ANXA2-ceramide-LC3B complex formation by wild-type <i>P. gingivalis</i> prevented ceramide-dependent mitophagy. Moreover, a FimA"],"journal":["iScience"],"pubmed_title":["Opportunistic pathogen <i>Porphyromonas gingivalis</i> targets the LC3B-ceramide complex and mediates lethal mitophagy resistance in oral tumors."],"pmcid":["PMC11108982"],"funding_grant_id":["P30 CA138313","R01 DE030313","P30 DK123704"],"pubmed_authors":["Engevik M","Ogretmen B","Wellslager B","Sheridan M","Oleinik N","Pandruvada S","Yilmaz O","Kassir MF","Lee HG","Peterson Y","Szulc ZM","Chowdhury N"],"additional_accession":[]},"is_claimable":false,"name":"Opportunistic pathogen <i>Porphyromonas gingivalis</i> targets the LC3B-ceramide complex and mediates lethal mitophagy resistance in oral tumors.","description":"Mechanisms by which <i>Porphyromonas gingivalis</i> (<i>P. gingivalis</i>) infection enhances oral tumor growth or resistance to cell death remain elusive. Here, we determined that <i>P. gingivalis</i> infection mediates therapeutic resistance via inhibiting lethal mitophagy in cancer cells and tumors. Mechanistically, <i>P. gingivalis</i> targets the LC3B-ceramide complex by associating with LC3B via bacterial major fimbriae (FimA) protein, preventing ceramide-dependent mitophagy in response to various therapeutic agents. Moreover, ceramide-mediated mitophagy is induced by Annexin A2 (ANXA2)-ceramide association involving the E142 residue of ANXA2. Inhibition of ANXA2-ceramide-LC3B complex formation by wild-type <i>P. gingivalis</i> prevented ceramide-dependent mitophagy. Moreover, a FimA","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-06-01T11:51:36.077Z","creation":"2026-04-08T11:59:35.555Z"},"accession":"S-EPMC11108982","cross_references":{"pubmed":["38779482"],"doi":["10.1016/j.isci.2024.109860"]}}