Histone-lysine N-methyltransferase 2D (KMT2D) impending therapeutic target for the management of cancer: The giant rats tail

Meshak Dhanashekaran Cecileya Jasmin, N Radhakrishnan, Venugopal Vinod Prabhu, Kunnathur Murugesan Sakthivel, Rasmi Rajan Radha
{"title":"Histone-lysine N-methyltransferase 2D (KMT2D) impending therapeutic target for the management of cancer: The giant rats tail","authors":"Meshak Dhanashekaran Cecileya Jasmin, N Radhakrishnan, Venugopal Vinod Prabhu, Kunnathur Murugesan Sakthivel, Rasmi Rajan Radha","doi":"10.1615/jenvironpatholtoxicoloncol.2024053872","DOIUrl":null,"url":null,"abstract":"The Histone-lysine N-methyltransferase 2D (KMT2D), tumor suppressor gene which is the major component of histone H3K4 mono-methyltransferase in mammals and has significant role in regulation of a gene which are frequently mutated that lead to many different types of cancers that includenon-Hodgkin lymphoma, medulloblastoma, prostate carcinoma, renal carcinoma, bladder carcinoma and lung carcinoma. KMT2D gene epigenetic alterations in histone methylation play a significant role for the initiation and progression of cancers from pre-cancerous lesions, yet its complete function in oncogenesis remains unsolved. KMT2D deficiency - loss are thought of initial mediators of cancer development and cell migration such as B‐cell lymphoma, medulloblastoma, melanoma, pancreas and lung cancer. The KMT2D loss has know to activate glycolytic genes that promote aggressive tumor progression. Therefore, the present review serves to underline the update on recent research pertaining toKMT2D gene, that could be a potential therapeutic target in down regulating glycolytic genes such as Pgk1,Ldha, Pgam1 and Gapdh; 2, tyrosine kinases EGFR - ERBB2, RTK-RAS signaling, Ras activator genes Rgl1, Rasgrp1, Rasgrf1, Rasgrf2 and Rapgef5 in suppressing the tumor progression that may represent novel targeted therapy for the management of cancer. This review will facilitate to understand the gene expression that inhibits cancer progression and which could serve as a potential molecular target in understanding cancer pathogenesis.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"4 1","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Environmental Pathology Toxicology and Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024053872","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The Histone-lysine N-methyltransferase 2D (KMT2D), tumor suppressor gene which is the major component of histone H3K4 mono-methyltransferase in mammals and has significant role in regulation of a gene which are frequently mutated that lead to many different types of cancers that includenon-Hodgkin lymphoma, medulloblastoma, prostate carcinoma, renal carcinoma, bladder carcinoma and lung carcinoma. KMT2D gene epigenetic alterations in histone methylation play a significant role for the initiation and progression of cancers from pre-cancerous lesions, yet its complete function in oncogenesis remains unsolved. KMT2D deficiency - loss are thought of initial mediators of cancer development and cell migration such as B‐cell lymphoma, medulloblastoma, melanoma, pancreas and lung cancer. The KMT2D loss has know to activate glycolytic genes that promote aggressive tumor progression. Therefore, the present review serves to underline the update on recent research pertaining toKMT2D gene, that could be a potential therapeutic target in down regulating glycolytic genes such as Pgk1,Ldha, Pgam1 and Gapdh; 2, tyrosine kinases EGFR - ERBB2, RTK-RAS signaling, Ras activator genes Rgl1, Rasgrp1, Rasgrf1, Rasgrf2 and Rapgef5 in suppressing the tumor progression that may represent novel targeted therapy for the management of cancer. This review will facilitate to understand the gene expression that inhibits cancer progression and which could serve as a potential molecular target in understanding cancer pathogenesis.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
组蛋白-赖氨酸 N-甲基转移酶 2D (KMT2D)即将成为治疗癌症的靶点:巨鼠尾巴
组蛋白-赖氨酸 N-甲基转移酶 2D(KMT2D)是哺乳动物中组蛋白 H3K4 单甲基转移酶的主要成分,是肿瘤抑制基因,在调控基因突变方面发挥着重要作用,而基因突变会导致多种不同类型的癌症,包括非霍奇金淋巴瘤、髓母细胞瘤、前列腺癌、肾癌、膀胱癌和肺癌。KMT2D 基因在组蛋白甲基化方面的表观遗传学改变对癌症从癌前病变到癌症的发生和发展起着重要作用,但它在致癌过程中的全部功能仍未得到解决。KMT2D 缺失被认为是癌症发展和细胞迁移的初始介质,如 B 细胞淋巴瘤、髓母细胞瘤、黑色素瘤、胰腺癌和肺癌。KMT2D缺失可激活糖酵解基因,促进侵袭性肿瘤进展。因此,本综述旨在强调与 KMT2D 基因有关的最新研究进展,KMT2D 基因可能是下调 Pgk1、Ldha、Pgam1 和 Gapdh 等糖酵解基因的潜在治疗靶点;2、酪氨酸激酶表皮生长因子受体(EGFR)- ERBB2、RTK-RAS 信号转导、Ras 激活基因 Rgl1、Rasgrp1、Rasgrf1、Rasgrf2 和 Rapgef5 在抑制肿瘤进展方面的作用,这可能是治疗癌症的新型靶向疗法。本综述将有助于了解抑制癌症进展的基因表达,这些基因可作为了解癌症发病机制的潜在分子靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
3.80
自引率
0.00%
发文量
20
审稿时长
>12 weeks
期刊介绍: The Journal of Environmental Pathology, Toxicology and Oncology publishes original research and reviews of factors and conditions that affect human and animal carcinogensis. Scientists in various fields of biological research, such as toxicologists, chemists, immunologists, pharmacologists, oncologists, pneumologists, and industrial technologists, will find this journal useful in their research on the interface between the environment, humans, and animals.
期刊最新文献
Ethyl Acetate Extract of Oratosquilla Inhibits the Growth of Nasopharyngeal Carcinoma through the Hippo Pathway Molecular mechanism of lncRNAs in ovarian cancer: lncRNA CASC19 regulates the malignant progression of ovarian cancer through miR-761/CBX2 axis LncRNA linc01105 inhibits gastric cancer growth and metastasis by regulating the miR-650/TCEA3 axis Identification of Lung Adenocarcinoma Subtypes by Using Growth Hormone-Releasing Hormone-Related Genes and Establishment of Signature to Predict Prognosis and Guide Immunother Analysis of the clinical value of hsa_circ_0001955 in papillary thyroid cancer treated with 131 iodine
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1