{"title":"<i>KMT2D</i> deficiency confers a therapeutic vulnerability to glycolytic and <i>IGFR</i> inhibitors in melanoma.","authors":"Navya Murugesan, Mayinuer Maitituoheti","doi":"10.1080/23723556.2021.1984827","DOIUrl":null,"url":null,"abstract":"<p><p>We reported that histone H3 lysine (K) 4 methyltransferase, <i>KMT2D</i>, serves as a potent tumor-suppressor in melanoma, which was identified via <i>in vivo</i> epigenome-focused RNA interference (RNAi) screen. <i>KMT2D</i>-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.6000,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/06/30/KMCO_8_1984827.PMC8632269.pdf","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and Cellular Oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23723556.2021.1984827","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 1
Abstract
We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway.
期刊介绍：
For a long time, solid neoplasms have been viewed as relatively homogeneous entities composed for the most part of malignant cells. It is now clear that tumors are highly heterogeneous structures that evolve in the context of intimate interactions between cancer cells and endothelial, stromal as well as immune cells. During the past few years, experimental and clinical oncologists have witnessed several conceptual transitions of this type. Molecular and Cellular Oncology (MCO) emerges within this conceptual framework as a high-profile forum for the publication of fundamental, translational and clinical research on cancer. The scope of MCO is broad. Submissions dealing with all aspects of oncogenesis, tumor progression and response to therapy will be welcome, irrespective of whether they focus on solid or hematological neoplasms. MCO has gathered leading scientists with expertise in multiple areas of cancer research and other fields of investigation to constitute a large, interdisciplinary, Editorial Board that will ensure the quality of articles accepted for publication. MCO will publish Original Research Articles, Brief Reports, Reviews, Short Reviews, Commentaries, Author Views (auto-commentaries) and Meeting Reports dealing with all aspects of cancer research.
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