{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nataraj NB"],"funding":["Advanced Medical Research Foundation","Dr. Miriam and Sheldon G. Adelson Medical Research Foundation","Cancer Research UK","European Research Council","Israel Science Foundation","National Institute for Health Research (NIHR)","NCI NIH HHS","Israel Cancer Research Fund"],"pagination":["110418"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8957480"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["38(8)"],"pubmed_abstract":["By establishing multi-omics pipelines, we uncover overexpression and gene copy-number alterations of nucleoporin-93 (NUP93), a nuclear pore component, in aggressive human mammary tumors. NUP93 overexpression enhances transendothelial migration and matrix invasion in vitro, along with tumor growth and metastasis in animal models. These findings are supported by analyses of two sets of naturally occurring mutations: rare oncogenic mutations and inactivating familial nephrotic syndrome mutations. Mechanistically, NUP93 binds with importins, boosts nuclear transport of importins' cargoes, such as β-catenin, and activates MYC. Likewise, NUP93 overexpression enhances the ultimate nuclear transport step shared by additional signaling pathways, including TGF-β/SMAD and EGF/ERK. The emerging addict"],"journal":["Cell reports"],"pubmed_title":["Nucleoporin-93 reveals a common feature of aggressive breast cancers: robust nucleocytoplasmic transport of transcription factors."],"pmcid":["PMC8957480"],"funding_grant_id":["R01 CA072981","29567","R37 CA072981","16942","NF-SI-0611-10154","NF-SI-0515-10090"],"pubmed_authors":["Livneh I","Noronha A","Yarden Y","Tarcitano E","Mohan Raju HR","Rueda O","Drago-Garcia D","Ciechanover A","Geiger T","Seger R","Caldas C","Lev S","Lee JS","Srivastava S","Ghosh S","Ulitsky I","Lindzen M","Selitrennik M","Nataraj NB","Sekar A","Zuckerman B","Ruppin E"],"additional_accession":[]},"is_claimable":false,"name":"Nucleoporin-93 reveals a common feature of aggressive breast cancers: robust nucleocytoplasmic transport of transcription factors.","description":"By establishing multi-omics pipelines, we uncover overexpression and gene copy-number alterations of nucleoporin-93 (NUP93), a nuclear pore component, in aggressive human mammary tumors. NUP93 overexpression enhances transendothelial migration and matrix invasion in vitro, along with tumor growth and metastasis in animal models. These findings are supported by analyses of two sets of naturally occurring mutations: rare oncogenic mutations and inactivating familial nephrotic syndrome mutations. Mechanistically, NUP93 binds with importins, boosts nuclear transport of importins' cargoes, such as β-catenin, and activates MYC. Likewise, NUP93 overexpression enhances the ultimate nuclear transport step shared by additional signaling pathways, including TGF-β/SMAD and EGF/ERK. The emerging addict","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-05-10T01:38:16.187Z","creation":"2025-02-19T01:12:01.353Z"},"accession":"S-EPMC8957480","cross_references":{"pubmed":["35196484"],"doi":["10.1016/j.celrep.2022.110418"]}}