{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T06:12:44Z","timestamp":1788415964790,"version":"build-2803163510"},"reference-count":91,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T00:00:00Z","timestamp":1788393600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Ubiquitination is a major regulatory process that is often dysregulated in carcinogenesis. The C-terminal to LisH (CTLH) complex is a multi-subunit E3 ubiquitin ligase that has been shown to exert tumor-promoting and tumor-suppressing functions. Its core scaffolding subunit, RanBP9, has been implicated in regulating oncogenic signaling, but it remains unclear whether RanBP9 loss promotes tumorigenesis\n                      <jats:italic>in vivo<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>This study aimed to evaluate the functional consequence of RanBP9 loss, alone or in combination with p53 deficiency, in mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mice with single or combined germline deletion of\n                      <jats:italic>Ranbp9<\/jats:italic>\n                      or\n                      <jats:italic>Trp53<\/jats:italic>\n                      , were generated and assessed for\n                      <jats:italic>in vivo<\/jats:italic>\n                      tumorigenesis. Tumors were characterized by histology and immunohistochemistry staining. Functional assays in mixed\n                      <jats:italic>Ranbp9<\/jats:italic>\n                      \/\n                      <jats:italic>Trp53<\/jats:italic>\n                      mouse embryonic fibroblasts (MEFs) were performed to evaluate proliferation and survival properties. Global label-free quantification (LFQ) proteomics was performed on MEFs to identify differentially expressed proteins. Genomic alterations of CTLH complex subunits were evaluated in sarcoma patients using the TCGA-SARC dataset.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Biallelic deletion of\n                      <jats:italic>Ranbp9<\/jats:italic>\n                      did not induce tumor development. In contrast, double heterozygous\n                      <jats:italic>Ranbp9<\/jats:italic>\n                      and\n                      <jats:italic>Trp53<\/jats:italic>\n                      (\n                      <jats:italic>\n                        R9\/p53\n                        <jats:sup>DHet<\/jats:sup>\n                      <\/jats:italic>\n                      ) mice exhibited earlier tumor onset and increased soft tissue sarcoma development compared with\n                      <jats:italic>Trp53<\/jats:italic>\n                      heterozygous (\n                      <jats:italic>\n                        p53\n                        <jats:sup>Het<\/jats:sup>\n                      <\/jats:italic>\n                      ) mice. Histopathological analysis revealed increased mitotic activity in\n                      <jats:italic>\n                        R9\/p53\n                        <jats:sup>DHet<\/jats:sup>\n                      <\/jats:italic>\n                      sarcomas with high Ki-67 and phospho-ERK expression. Functional and proteomic characterization of\n                      <jats:italic>\n                        R9\/p53\n                        <jats:sup>DHet<\/jats:sup>\n                      <\/jats:italic>\n                      MEFs demonstrated increased proliferative capacity and changes in proteomic landscape in proteins involved in DNA replication, cell cycle, and metabolism. Finally, TCGA-SARC analysis showed that that low mRNA expression of CTLH catalytic subunit\n                      <jats:italic>RMND5B<\/jats:italic>\n                      correlated significantly with reduced overall survival.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Loss of RanBP9 induces deregulation of signaling cascades, and combined with p53 deficiency, further promotes sarcoma development in mice. This mouse model provides a valuable platform to further study pathways and candidates regulated by the CTLH complex in sarcoma biology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fonc.2026.1743582","type":"journal-article","created":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T05:15:28Z","timestamp":1788412528000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Loss of RanBP9 cooperates with p53 deficiency to promote sarcomagenesis"],"prefix":"10.3389","volume":"16","author":[{"given":"Brianna C.","family":"Gonga-Cav\u00e9","sequence":"first","affiliation":[{"name":"Robarts Research Institute, University of Western Ontario","place":["London, ON, Canada"]},{"name":"Department of Biochemistry, Schulich School of Medicine and Dentistry, University of Western Ontario","place":["London, ON, 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