{"title":"Multi-omics analysis identifies OSGEPL1 as an oncogene in hepatocellular carcinoma.","authors":"Sintim Mui, Juanyi Shi, Kai Wen, Yongcong Yan, Huoming Li, Weidong Wang, Zhenyu Zhou, Zhiyu Xiao","doi":"10.1007/s12672-025-02066-5","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>N6-Threonylcarbamoyladenosine (t<sup>6</sup>A) modification irregularities and their associated enzymes genes (OSGEP, OSGEPL1, TPRKB, GON7, TP53RK, YRDC, and LAGE3) are linked to various malignancies development, including Hepatocellular Carcinoma (HCC), yet the specific mechanisms remain obscure. This gap in knowledge is significant, as understanding the mechanisms of t<sup>6</sup>A modification could reveal new insights into HCC pathogenesis and potentially identify novel therapeutic targets.</p><p><strong>Methods: </strong>We leveraged data from The Cancer Genome Atlas (TCGA) to analyze the expression of t<sup>6</sup>A-associated genes, with a focus on OSGEPL1 in HCC. Our analyses included survival outcome, gene expression, functional enrichment, immune cell infiltration, and somatic mutation data.</p><p><strong>Results: </strong>We discovered that OSGEPL1 is upregulated in HCC and is correlated with tumor grade, pathological T stage, and overall stage. It inversely impacts overall survival and immune cell infiltration. In vitro experiments confirmed the role of OSGEPL1 in promoting HCC cell proliferation.</p><p><strong>Conclusions: </strong>This study implicates t<sup>6</sup>A modification pathway dysregulation in HCC prognosis, identifying OSGEPL1 as a potential therapeutic target. These findings provide novel insights into HCC pathogenesis and may guide future treatment strategies.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"328"},"PeriodicalIF":2.8000,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911280/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Discover. Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12672-025-02066-5","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: N6-Threonylcarbamoyladenosine (t6A) modification irregularities and their associated enzymes genes (OSGEP, OSGEPL1, TPRKB, GON7, TP53RK, YRDC, and LAGE3) are linked to various malignancies development, including Hepatocellular Carcinoma (HCC), yet the specific mechanisms remain obscure. This gap in knowledge is significant, as understanding the mechanisms of t6A modification could reveal new insights into HCC pathogenesis and potentially identify novel therapeutic targets.
Methods: We leveraged data from The Cancer Genome Atlas (TCGA) to analyze the expression of t6A-associated genes, with a focus on OSGEPL1 in HCC. Our analyses included survival outcome, gene expression, functional enrichment, immune cell infiltration, and somatic mutation data.
Results: We discovered that OSGEPL1 is upregulated in HCC and is correlated with tumor grade, pathological T stage, and overall stage. It inversely impacts overall survival and immune cell infiltration. In vitro experiments confirmed the role of OSGEPL1 in promoting HCC cell proliferation.
Conclusions: This study implicates t6A modification pathway dysregulation in HCC prognosis, identifying OSGEPL1 as a potential therapeutic target. These findings provide novel insights into HCC pathogenesis and may guide future treatment strategies.