{"title":"Clinical and Prognostic Values of DNMT3B Expression in Hepatocellular Carcinoma","authors":"Jongwan Kim, Jae-Hee Park, Jae-Ho Lee","doi":"10.46308/kmj.2022.00045","DOIUrl":null,"url":null,"abstract":"De novo methylation is occurred frequently during the early embryogenesis and is faithfully copied following DNA replication at each cell cycle [1]. DNA methylation is involved in many embryonic developments, biological processes, and cell differentiation [2]. The dysregulation of DNA methyltransferases (DNMTs) and subsequent aberrant DNA methylation is a key feature of human malignancies [3,4]. DNMT1, DNMT3A, and DNMT3B are the enzymatic players of DNA methylation [1,2]. DNMT3B overexpression is frequently found in tumors, especially in 30% of breast cancers [5,6]. And it result into variation in the targeting efficiency and abnormal catalytic activity contributing to cancer development and progression. Therefore, DNMT3B may act as an oncogene, and its overexpression induces an unfavorable prognosis [3-6]. Hepatocellular carcinoma (HCC) is a majority of human cancers in worldwide, and is a leading cause of death in Korea [7,8]. Recent studies about HCC showed an alteration of DNA methylation by dysregulation of DNMT3B [9,10]. Yu et al. described that telomerase reverse transcriptase (TERT) regulates DNMT3B expression in HCC and their co-operation may predict a poorer prognosis [11]. Recent advances in genomic profiling using next-generation sequencing have made it possible to identify the genetic characteristics of cancer. Large-scale cancer genome studies such as The Cancer Genome Atlas (TCGA) used to investigate genes in different cancer types [12]. However, clinicopathopISSN 2092-8335 · eISSN 2733-5380 Keimyung Med J 2021[Epub ahead of print] https://doi.org/10.46308/kmj.2022.00045 Original Article","PeriodicalId":166951,"journal":{"name":"Keimyung Medical Journal","volume":"21 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2022-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Keimyung Medical Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.46308/kmj.2022.00045","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
De novo methylation is occurred frequently during the early embryogenesis and is faithfully copied following DNA replication at each cell cycle [1]. DNA methylation is involved in many embryonic developments, biological processes, and cell differentiation [2]. The dysregulation of DNA methyltransferases (DNMTs) and subsequent aberrant DNA methylation is a key feature of human malignancies [3,4]. DNMT1, DNMT3A, and DNMT3B are the enzymatic players of DNA methylation [1,2]. DNMT3B overexpression is frequently found in tumors, especially in 30% of breast cancers [5,6]. And it result into variation in the targeting efficiency and abnormal catalytic activity contributing to cancer development and progression. Therefore, DNMT3B may act as an oncogene, and its overexpression induces an unfavorable prognosis [3-6]. Hepatocellular carcinoma (HCC) is a majority of human cancers in worldwide, and is a leading cause of death in Korea [7,8]. Recent studies about HCC showed an alteration of DNA methylation by dysregulation of DNMT3B [9,10]. Yu et al. described that telomerase reverse transcriptase (TERT) regulates DNMT3B expression in HCC and their co-operation may predict a poorer prognosis [11]. Recent advances in genomic profiling using next-generation sequencing have made it possible to identify the genetic characteristics of cancer. Large-scale cancer genome studies such as The Cancer Genome Atlas (TCGA) used to investigate genes in different cancer types [12]. However, clinicopathopISSN 2092-8335 · eISSN 2733-5380 Keimyung Med J 2021[Epub ahead of print] https://doi.org/10.46308/kmj.2022.00045 Original Article