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      H3K36 trimethylation-mediated biological functions in cancer

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          Abstract

          Histone modification is an important form of epigenetic regulation. Thereinto, histone methylation is a critical determination of chromatin states, participating in multiple cellular processes. As a conserved histone methylation mark, histone 3 lysine 36 trimethylation (H3K36me3) can mediate multiple transcriptional-related events, such as the regulation of transcriptional activity, transcription elongation, pre-mRNA alternative splicing, and RNA m 6A methylation. Additionally, H3K36me3 also contributes to DNA damage repair. Given the crucial function of H3K36me3 in genome regulation, the roles of H3K36me3 and its sole methyltransferase SETD2 in pathogenesis, especially malignancies, have been emphasized in many studies, and it is conceivable that disruption of histone methylation regulatory network composed of “writer”, “eraser”, “reader”, and the mutation of H3K36me3 codes have the capacity of powerfully modulating cancer initiation and development. Here we review H3K36me3-mediated biological processes and summarize the latest findings regarding its role in cancers. We highlight the significance of epigenetic combination therapies in cancers.

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          Chromatin modifications and their function.

          Tony Kouzarides (2007)
          The surface of nucleosomes is studded with a multiplicity of modifications. At least eight different classes have been characterized to date and many different sites have been identified for each class. Operationally, modifications function either by disrupting chromatin contacts or by affecting the recruitment of nonhistone proteins to chromatin. Their presence on histones can dictate the higher-order chromatin structure in which DNA is packaged and can orchestrate the ordered recruitment of enzyme complexes to manipulate DNA. In this way, histone modifications have the potential to influence many fundamental biological processes, some of which may be epigenetically inherited.
          Article 0 comments Cited 948 times – based on 0 reviews     Review now
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            Targeting EZH2 in cancer.

            Kimberly H Kim, Charles Roberts (2016)
            Recent genomic studies have resulted in an emerging understanding of the role of chromatin regulators in the development of cancer. EZH2, a histone methyl transferase subunit of a Polycomb repressor complex, is recurrently mutated in several forms of cancer and is highly expressed in numerous others. Notably, both gain-of-function and loss-of-function mutations occur in cancers but are associated with distinct cancer types. Here we review the spectrum of EZH2-associated mutations, discuss the mechanisms underlying EZH2 function, and synthesize a unifying perspective that the promotion of cancer arises from disruption of the role of EZH2 as a master regulator of transcription. We further discuss EZH2 inhibitors that are now showing early signs of promise in clinical trials and also additional strategies to combat roles of EZH2 in cancer.
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              Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse.

              Sunil R Hingorani, Emanuel Petricoin, Anirban Maitra … (2003)
              To evaluate the role of oncogenic RAS mutations in pancreatic tumorigenesis, we directed endogenous expression of KRAS(G12D) to progenitor cells of the mouse pancreas. We find that physiological levels of Kras(G12D) induce ductal lesions that recapitulate the full spectrum of human pancreatic intraepithelial neoplasias (PanINs), putative precursors to invasive pancreatic cancer. The PanINs are highly proliferative, show evidence of histological progression, and activate signaling pathways normally quiescent in ductal epithelium, suggesting potential therapeutic and chemopreventive targets for the cognate human condition. At low frequency, these lesions also progress spontaneously to invasive and metastatic adenocarcinomas, establishing PanINs as definitive precursors to the invasive disease. Finally, mice with PanINs have an identifiable serum proteomic signature, suggesting a means of detecting the preinvasive state in patients.
              Article 0 comments Cited 528 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Chunxiang Li: lichunxiang@cicams.ac.cn
                Jie He:
                ORCID: http://orcid.org/0000-0003-0327-8852
                prof.jiehe@gmail.com
                Journal
                Journal ID (nlm-ta): Clin Epigenetics
                Journal ID (iso-abbrev): Clin Epigenetics
                Title: Clinical Epigenetics
                Publisher: BioMed Central (London )
                ISSN (Print): 1868-7075
                ISSN (Electronic): 1868-7083
                Publication date (Electronic): 29 October 2021
                Publication date PMC-release: 29 October 2021
                Publication date Collection: 2021
                Volume: 13
                Electronic Location Identifier: 199
                Affiliations
                [1 ]GRID grid.506261.6, ISNI 0000 0001 0706 7839, Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, , Chinese Academy of Medical Sciences and Peking Union Medical College, ; Beijing, 100021 China
                [2 ]GRID grid.506261.6, ISNI 0000 0001 0706 7839, Department of Colorectal Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, , Chinese Academy of Medical Sciences and Peking Union Medical College, ; Beijing, 100021 China
                Author information
                http://orcid.org/0000-0003-0327-8852
                Article
                Publisher ID: 1187
                DOI: 10.1186/s13148-021-01187-2
                PMC ID: 8555273
                PubMed ID: 34715919
                SO-VID: 6221e612-2214-4f48-9bd9-87a45b8b8944
                Copyright © © The Author(s) 2021
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 20 September 2021
                Date accepted : 19 October 2021
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81972196
                Award Recipient :
                Funded by: National Key R&D Program of China
                Award ID: 2020AAA0109505
                Award Recipient :
                Funded by: R&D Program of Beijing Municipal Education Commission
                Award ID: KJZD20191002302
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Genetics
                Keywords: histone modification,h3k36me3,solid tumor,epigenetic therapy
                Data availability:
                ScienceOpen disciplines: Genetics
                Keywords: histone modification, h3k36me3, solid tumor, epigenetic therapy

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