{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang B"],"funding":["Department of Science and Technology of Guangdong Province","Science, Technology and Innovation Commission of Shenzhen Municipality","Guangdong Basic and Applied Basic Research Foundation","Foundation for the National Institutes of Health","Department of Defense Prostate Cancer Research Program","National Natural Science Foundation of China","NCI NIH HHS"],"pagination":["e175949"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11245161"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(14)"],"pubmed_abstract":["Inactivation of phosphatase and tensin homolog (PTEN) is prevalent in human prostate cancer and causes high-grade adenocarcinoma with a long latency. Cancer-associated fibroblasts (CAFs) play a pivotal role in tumor progression, but it remains elusive whether and how PTEN-deficient prostate cancers reprogram CAFs to overcome the barriers for tumor progression. Here, we report that PTEN deficiency induced Krüppel-like factor 5 (KLF5) acetylation and that interruption of KLF5 acetylation orchestrated intricate interactions between cancer cells and CAFs that enhance FGF receptor 1 (FGFR1) signaling and promote tumor growth. Deacetylated KLF5 promoted tumor cells to secrete TNF-α, which stimulated inflammatory CAFs to release FGF9. CX3CR1 inhibition blocked FGFR1 activation triggered by FGF9 a"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Interruption of KLF5 acetylation promotes PTEN-deficient prostate cancer progression by reprogramming cancer-associated fibroblasts."],"pmcid":["PMC11245161"],"funding_grant_id":["2021QN02Y875","2021A1515110051","JCYJ20220530113609020,JCYJ20200109141229255,20200925174802001","P30 CA138292","R01 CA171189","R01CA171189","W81XWH-18-1-0526","82273079,82303045"],"pubmed_authors":["Barwick BG","Liu M","Du X","Dong JT","Zhou W","Xia S","Huang Q","Mai F","Li X","Ding W","Li Y","Osunkoya AO","Wang W","Chen Y","Zhang B","Ni JJ"],"additional_accession":[]},"is_claimable":false,"name":"Interruption of KLF5 acetylation promotes PTEN-deficient prostate cancer progression by reprogramming cancer-associated fibroblasts.","description":"Inactivation of phosphatase and tensin homolog (PTEN) is prevalent in human prostate cancer and causes high-grade adenocarcinoma with a long latency. Cancer-associated fibroblasts (CAFs) play a pivotal role in tumor progression, but it remains elusive whether and how PTEN-deficient prostate cancers reprogram CAFs to overcome the barriers for tumor progression. Here, we report that PTEN deficiency induced Krüppel-like factor 5 (KLF5) acetylation and that interruption of KLF5 acetylation orchestrated intricate interactions between cancer cells and CAFs that enhance FGF receptor 1 (FGFR1) signaling and promote tumor growth. Deacetylated KLF5 promoted tumor cells to secrete TNF-α, which stimulated inflammatory CAFs to release FGF9. CX3CR1 inhibition blocked FGFR1 activation triggered by FGF9 a","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-03T03:07:56.333Z","creation":"2025-04-04T08:04:08.752Z"},"accession":"S-EPMC11245161","cross_references":{"pubmed":["38781024"],"doi":["10.1172/JCI175949"]}}