Cited 2 times in
USO1 isoforms differentially promote liver cancer progression by dysregulating the ER-Golgi network
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 박영년 | - |
dc.date.accessioned | 2022-11-24T00:35:13Z | - |
dc.date.available | 2022-11-24T00:35:13Z | - |
dc.date.issued | 2021-10 | - |
dc.identifier.issn | 0143-3334 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/190786 | - |
dc.description.abstract | Alternative splicing of RNA transcripts plays an important role in cancer development and progression. Recent advances in RNA-seq technology have made it possible to identify alternately spliced events in various types of cancer; however, research on hepatocellular carcinoma (HCC) is still limited. Here, by performing RNA-seq profiling of HCC transcripts at isoform level, we identified tumor-specific and molecular subtype-dependent expression of the USO1 isoforms, which we designated as a normal form USO1-N (XM_001290049) and a tumor form USO1-T (NM_003715). The expression of USO1-T, but not USO1-N, was associated with worse prognostic outcomes of HCC patients. We confirmed that the expression of USO1-T promoted an aggressive phenotype of HCC, both in vitro and in vivo. In addition, structural modeling analyses revealed that USO1-T lacks an ARM10 loop encoded by exon 15, which may weaken the dimerization of USO1 and its tethering to GM130. We demonstrated that USO1-T ensured unstacking of the Golgi and accelerated the vesicles trafficking from endoplasmic reticulum (ER) to Golgi and plasma membrane in multiple liver cancer cells. ERK and GRASP65 were found to be involved in the USO1-T-mediated Golgi dysfunction. Conclusively, we provide new mechanophysical insights into the USO1 isoforms that differentially regulate the ER-Golgi network, promoting the heterogeneous HCC progression. | - |
dc.description.statementOfResponsibility | open | - |
dc.language | English | - |
dc.publisher | Irl Press At Oxford University Press | - |
dc.relation.isPartOf | CARCINOGENESIS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | Carcinoma, Hepatocellular / metabolism | - |
dc.subject.MESH | Carcinoma, Hepatocellular / pathology* | - |
dc.subject.MESH | Disease Progression | - |
dc.subject.MESH | Endoplasmic Reticulum / metabolism* | - |
dc.subject.MESH | Exons | - |
dc.subject.MESH | Golgi Apparatus / metabolism* | - |
dc.subject.MESH | Golgi Matrix Proteins / genetics | - |
dc.subject.MESH | Golgi Matrix Proteins / metabolism* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Liver Neoplasms / metabolism | - |
dc.subject.MESH | Liver Neoplasms / pathology* | - |
dc.subject.MESH | Protein Isoforms / genetics | - |
dc.subject.MESH | Protein Isoforms / metabolism | - |
dc.subject.MESH | Protein Multimerization | - |
dc.subject.MESH | Protein Transport | - |
dc.subject.MESH | RNA Splicing | - |
dc.subject.MESH | Vesicular Transport Proteins / genetics | - |
dc.subject.MESH | Vesicular Transport Proteins / metabolism* | - |
dc.title | USO1 isoforms differentially promote liver cancer progression by dysregulating the ER-Golgi network | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pathology (병리학교실) | - |
dc.contributor.googleauthor | Sarah Yoon | - |
dc.contributor.googleauthor | Ji-Hye Choi | - |
dc.contributor.googleauthor | Masaud Shah | - |
dc.contributor.googleauthor | So Mee Kwon | - |
dc.contributor.googleauthor | Jieun Yang | - |
dc.contributor.googleauthor | Young Nyun Park | - |
dc.contributor.googleauthor | Hee-Jung Wang | - |
dc.contributor.googleauthor | Hyun Goo Woo | - |
dc.identifier.doi | 10.1093/carcin/bgab067 | - |
dc.contributor.localId | A01563 | - |
dc.relation.journalcode | J00456 | - |
dc.identifier.eissn | 1460-2180 | - |
dc.identifier.pmid | 34293111 | - |
dc.identifier.url | https://academic.oup.com/carcin/article/42/9/1208/6325611 | - |
dc.contributor.alternativeName | Park, Young Nyun | - |
dc.contributor.affiliatedAuthor | 박영년 | - |
dc.citation.volume | 42 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 1208 | - |
dc.citation.endPage | 1220 | - |
dc.identifier.bibliographicCitation | CARCINOGENESIS, Vol.42(9) : 1208-1220, 2021-10 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.