{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Weissenrieder JS"],"funding":["NIDDK NIH HHS","NIAID NIH HHS","Foundation for the National Institutes of Health","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["115627"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12857258"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(5)"],"pubmed_abstract":["Endoplasmic reticulum to mitochondria Ca<sup>2+</sup> transfer is important for cancer cell survival, but the role of mitochondrial Ca<sup>2+</sup> uptake through the mitochondrial Ca<sup>2+</sup> uniporter (MCU) in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. Here, we show that increased MCU expression is associated with malignancy and poorer outcomes in patients with PDAC. In isogenic murine PDAC models, Mcu deletion (Mcu<sup>KO</sup>) ablated mitochondrial Ca<sup>2+</sup> uptake, which reduced proliferation and inhibited self-renewal. Orthotopic implantation of MCU-null tumor cells reduced primary tumor growth and metastasis. Mcu deletion reduced the cellular plasticity of tumor cells by inhibiting epithelial-to-mesenchymal transition (EMT), which contributes to metasta"],"journal":["Cell reports"],"pubmed_title":["Mitochondrial Ca<sup>2+</sup> controls pancreatic cancer growth and metastasis by regulating epithelial cell plasticity."],"pmcid":["PMC12857258"],"funding_grant_id":["R01 CA250173","R00 CA252153","T32 AI095213","P30 DK050306","T32 GM135751","F32 CA250144"],"pubmed_authors":["Pitarresi JR","Drager R","Simin K","Bhalerao N","Peura J","Foskett JK","Stanger BZ","Ruscetti M","Rustgi AK","Paudel U","Furth EE","Johnson C","Weissenrieder JS","Weinmann N","Wengyn M"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial Ca<sup>2+</sup> controls pancreatic cancer growth and metastasis by regulating epithelial cell plasticity.","description":"Endoplasmic reticulum to mitochondria Ca<sup>2+</sup> transfer is important for cancer cell survival, but the role of mitochondrial Ca<sup>2+</sup> uptake through the mitochondrial Ca<sup>2+</sup> uniporter (MCU) in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. Here, we show that increased MCU expression is associated with malignancy and poorer outcomes in patients with PDAC. In isogenic murine PDAC models, Mcu deletion (Mcu<sup>KO</sup>) ablated mitochondrial Ca<sup>2+</sup> uptake, which reduced proliferation and inhibited self-renewal. Orthotopic implantation of MCU-null tumor cells reduced primary tumor growth and metastasis. Mcu deletion reduced the cellular plasticity of tumor cells by inhibiting epithelial-to-mesenchymal transition (EMT), which contributes to metasta","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-12T10:10:55.993Z","creation":"2026-06-12T03:12:54.898Z"},"accession":"S-EPMC12857258","cross_references":{"pubmed":["40286270"],"doi":["10.1016/j.celrep.2025.115627"]}}