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USO1 isoforms differentially promote liver cancer progression by dysregulating the ER-Golgi network

DC Field Value Language
dc.contributor.author박영년-
dc.date.accessioned2022-11-24T00:35:13Z-
dc.date.available2022-11-24T00:35:13Z-
dc.date.issued2021-10-
dc.identifier.issn0143-3334-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/190786-
dc.description.abstractAlternative 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.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherIrl Press At Oxford University Press-
dc.relation.isPartOfCARCINOGENESIS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHCarcinoma, Hepatocellular / metabolism-
dc.subject.MESHCarcinoma, Hepatocellular / pathology*-
dc.subject.MESHDisease Progression-
dc.subject.MESHEndoplasmic Reticulum / metabolism*-
dc.subject.MESHExons-
dc.subject.MESHGolgi Apparatus / metabolism*-
dc.subject.MESHGolgi Matrix Proteins / genetics-
dc.subject.MESHGolgi Matrix Proteins / metabolism*-
dc.subject.MESHHumans-
dc.subject.MESHLiver Neoplasms / metabolism-
dc.subject.MESHLiver Neoplasms / pathology*-
dc.subject.MESHProtein Isoforms / genetics-
dc.subject.MESHProtein Isoforms / metabolism-
dc.subject.MESHProtein Multimerization-
dc.subject.MESHProtein Transport-
dc.subject.MESHRNA Splicing-
dc.subject.MESHVesicular Transport Proteins / genetics-
dc.subject.MESHVesicular Transport Proteins / metabolism*-
dc.titleUSO1 isoforms differentially promote liver cancer progression by dysregulating the ER-Golgi network-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학교실)-
dc.contributor.googleauthorSarah Yoon-
dc.contributor.googleauthorJi-Hye Choi-
dc.contributor.googleauthorMasaud Shah-
dc.contributor.googleauthorSo Mee Kwon-
dc.contributor.googleauthorJieun Yang-
dc.contributor.googleauthorYoung Nyun Park-
dc.contributor.googleauthorHee-Jung Wang-
dc.contributor.googleauthorHyun Goo Woo-
dc.identifier.doi10.1093/carcin/bgab067-
dc.contributor.localIdA01563-
dc.relation.journalcodeJ00456-
dc.identifier.eissn1460-2180-
dc.identifier.pmid34293111-
dc.identifier.urlhttps://academic.oup.com/carcin/article/42/9/1208/6325611-
dc.contributor.alternativeNamePark, Young Nyun-
dc.contributor.affiliatedAuthor박영년-
dc.citation.volume42-
dc.citation.number9-
dc.citation.startPage1208-
dc.citation.endPage1220-
dc.identifier.bibliographicCitationCARCINOGENESIS, Vol.42(9) : 1208-1220, 2021-10-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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