{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gomes AP"],"funding":["European Research Council","NIA NIH HHS","NCI NIH HHS"],"pagination":["435-443"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9050834"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4(4)"],"pubmed_abstract":["The alteration of metabolic pathways is a critical strategy for cancer cells to attain the traits necessary for metastasis in disease progression. Here, we find that dysregulation of propionate metabolism produces a pro-aggressive signature in breast and lung cancer cells, increasing their metastatic potential. This occurs through the downregulation of methylmalonyl coenzyme A epimerase (MCEE), mediated by an extracellular signal-regulated kinase 2-driven transcription factor Sp1/early growth response protein 1 transcriptional switch driven by metastatic signalling at its promoter level. The loss of MCEE results in reduced propionate-driven anaplerotic flux and intracellular and intratumoral accumulation of methylmalonic acid, a by-product of propionate metabolism that promotes cancer cell"],"journal":["Nature metabolism"],"pubmed_title":["Altered propionate metabolism contributes to tumour progression and aggressiveness."],"pmcid":["PMC9050834"],"funding_grant_id":["F31 CA220750","R35 CA197588","R00 CA218686","DP2 AG077698","R01 CA046595","711486","P01 CA120964"],"pubmed_authors":["Drapela S","Blenis J","Schild T","Ilter D","Fendt SM","Low V","Elia I","Mutvei AP","Nunes JB","Mullarky E","Rosenzweig A","Nagiec M","Schaffer BE","Gomes AP","Asara JM","Cantley LC","Han J","Broekaert D"],"additional_accession":[]},"is_claimable":false,"name":"Altered propionate metabolism contributes to tumour progression and aggressiveness.","description":"The alteration of metabolic pathways is a critical strategy for cancer cells to attain the traits necessary for metastasis in disease progression. Here, we find that dysregulation of propionate metabolism produces a pro-aggressive signature in breast and lung cancer cells, increasing their metastatic potential. This occurs through the downregulation of methylmalonyl coenzyme A epimerase (MCEE), mediated by an extracellular signal-regulated kinase 2-driven transcription factor Sp1/early growth response protein 1 transcriptional switch driven by metastatic signalling at its promoter level. The loss of MCEE results in reduced propionate-driven anaplerotic flux and intracellular and intratumoral accumulation of methylmalonic acid, a by-product of propionate metabolism that promotes cancer cell","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2025-05-18T12:50:04.805Z","creation":"2025-02-19T03:24:14.321Z"},"accession":"S-EPMC9050834","cross_references":{"pubmed":["35361954"],"doi":["10.1038/s42255-022-00553-5"]}}