癌症表观遗传学：肿瘤异质性、干细胞样状态的可塑性和耐药性。
Cancer epigenetics: tumor heterogeneity, plasticity of stem-like states, and drug resistance.
机构信息
The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
出版信息
Mol Cell. 2014 Jun 5;54(5):716-27. doi: 10.1016/j.molcel.2014.05.015.
Abstract
The existence of subpopulations of cells in cancers with increased tumor-initiating capacities and self-renewal potential, often termed "cancer stem cells," is a much discussed and key area of cancer biology. Such cellular heterogeneity is very important because of its impact on therapy and especially states of treatment resistance. A major question is whether there is plasticity for evolution of these cell states during tumorigenesis that can involve movement between cell populations in a reversible fashion. In this review, we discuss the possible role of epigenetic abnormalities as well as genetic alterations in such dynamics and in the creation of cellular heterogeneity in cancers of all types.
摘要
肿瘤中存在具有更高肿瘤起始能力和自我更新潜能的细胞亚群，通常被称为“肿瘤干细胞”，这是癌症生物学中一个备受讨论的关键领域。这种细胞异质性非常重要，因为它会影响治疗效果，特别是对治疗抵抗状态的影响。一个主要问题是，在肿瘤发生过程中，这些细胞状态是否存在可进化的可塑性，是否可以以可逆的方式在细胞群体之间移动。在这篇综述中，我们讨论了表观遗传异常以及遗传改变在这种动态变化和所有类型癌症中细胞异质性形成中的可能作用。
相似文献
1
Cancer epigenetics: tumor heterogeneity, plasticity of stem-like states, and drug resistance.癌症表观遗传学：肿瘤异质性、干细胞样状态的可塑性和耐药性。
Mol Cell. 2014 Jun 5;54(5):716-27. doi: 10.1016/j.molcel.2014.05.015.
2
Epigenetics and metabolism at the crossroads of stress-induced plasticity, stemness and therapeutic resistance in cancer.应激诱导可塑性、干性和癌症治疗抵抗中的表观遗传学和代谢交汇点。
Theranostics. 2020 May 15;10(14):6261-6277. doi: 10.7150/thno.42523. eCollection 2020.
3
Stem cell programs in cancer initiation, progression, and therapy resistance.肿瘤起始、进展和治疗抵抗中的干细胞程序。
Theranostics. 2020 Jul 9;10(19):8721-8743. doi: 10.7150/thno.41648. eCollection 2020.
4
Perturbation-Driven Entropy as a Source of Cancer Cell Heterogeneity.扰动驱动的熵是癌细胞异质性的一个来源。
Trends Cancer. 2020 Jun;6(6):454-461. doi: 10.1016/j.trecan.2020.02.016. Epub 2020 Mar 13.
5
Addressing intra-tumoral heterogeneity and therapy resistance.解决肿瘤内异质性和治疗抗性问题。
Oncotarget. 2016 Nov 1;7(44):72322-72342. doi: 10.18632/oncotarget.11875.
6
Emerging Mechanisms by which EMT Programs Control Stemness.EMT 程序控制干细胞特性的新兴机制。
Trends Cancer. 2020 Sep;6(9):775-780. doi: 10.1016/j.trecan.2020.03.011. Epub 2020 Apr 17.
7
Noncoding RNAs in Cancer Cell Plasticity.癌细胞可塑性中的非编码RNA
Adv Exp Med Biol. 2016;927:173-89. doi: 10.1007/978-981-10-1498-7_6.
8
Intratumoral Heterogeneity: From Diversity Comes Resistance.肿瘤内异质性：多样性导致耐药性。
Clin Cancer Res. 2015 Jul 1;21(13):2916-23. doi: 10.1158/1078-0432.CCR-14-1213. Epub 2015 Apr 2.
9
Drug resistance, epigenetics, and tumor cell heterogeneity.耐药性、表观遗传学和肿瘤细胞异质性。
Sci Transl Med. 2010 Apr 21;2(28):28ps19. doi: 10.1126/scitranslmed.3001056.
10
Loss of insulin-like growth factor II imprinting is a hallmark associated with enhanced chemo/radiotherapy resistance in cancer stem cells.胰岛素样生长因子II印记缺失是癌症干细胞中与化疗/放疗耐药性增强相关的一个标志。
Oncotarget. 2016 Aug 9;7(32):51349-51364. doi: 10.18632/oncotarget.9784.
引用本文的文献
1
Cell reprogramming in cancer: Interplay of genetic, epigenetic mechanisms, and the tumor microenvironment in carcinogenesis and metastasis.癌症中的细胞重编程：遗传、表观遗传机制以及肿瘤微环境在致癌作用和转移过程中的相互作用
World J Clin Oncol. 2025 Aug 24;16(8):106838. doi: 10.5306/wjco.v16.i8.106838.
2
LSGI: interpretable spatial gradient analysis for spatial transcriptomics data.LSGI：用于空间转录组学数据的可解释空间梯度分析
Genome Biol. 2025 Aug 8;26(1):238. doi: 10.1186/s13059-025-03716-1.
3
Joint representation and visualization of derailed cell states with Decipher.使用Decipher对脱轨细胞状态进行联合表示和可视化。
Genome Biol. 2025 Jul 23;26(1):219. doi: 10.1186/s13059-025-03682-8.
4
Long interspersed nuclear element 1 methylation in non-small cell lung cancer: implications for diagnosis, prognosis, and therapeutic targeting.非小细胞肺癌中长散在核元件1甲基化：对诊断、预后及治疗靶点的意义
Cell Commun Signal. 2025 Jul 22;23(1):350. doi: 10.1186/s12964-025-02343-4.
5
Cancer stem cells: Bridging microenvironmental interactions and clinical therapy.癌症干细胞：连接微环境相互作用与临床治疗
Clin Transl Med. 2025 Jul;15(7):e70406. doi: 10.1002/ctm2.70406.
6
G-quadruplex structures regulate long-range transcriptional reprogramming to promote drug resistance in ovarian cancer cells.G-四链体结构调控远距离转录重编程以促进卵巢癌细胞的耐药性。
Genome Biol. 2025 Jul 12;26(1):183. doi: 10.1186/s13059-025-03654-y.
7
Hippo pathway controls biopterin metabolism to shield adjacent cells from ferroptosis in lung cancer.河马通路控制生物蝶呤代谢，以保护肺癌中的相邻细胞免受铁死亡。
EMBO Rep. 2025 Jul 7. doi: 10.1038/s44319-025-00515-4.
8
27-Hydroxycholesterol in cancer development and drug resistance.27-羟基胆固醇在癌症发生发展及耐药性中的作用
J Enzyme Inhib Med Chem. 2025 Dec;40(1):2507670. doi: 10.1080/14756366.2025.2507670. Epub 2025 May 22.
9
Application of biomechanics in tumor epigenetic research.生物力学在肿瘤表观遗传学研究中的应用。
Mechanobiol Med. 2024 Aug 22;2(4):100093. doi: 10.1016/j.mbm.2024.100093. eCollection 2024 Dec.
10
The SGK3/GSK3β/β-catenin signaling promotes breast cancer stemness and confers resistance to alpelisib therapy.SGK3/GSK3β/β-连环蛋白信号通路促进乳腺癌干性并赋予对阿培利司治疗的抗性。
Int J Biol Sci. 2025 Mar 19;21(6):2462-2475. doi: 10.7150/ijbs.104850. eCollection 2025.
本文引用的文献
1
Age-related epigenetic drift in the pathogenesis of MDS and AML.与年龄相关的表观遗传漂变在骨髓增生异常综合征和急性髓系白血病发病机制中的作用
Genome Res. 2014 Apr;24(4):580-91. doi: 10.1101/gr.157529.113. Epub 2014 Jan 10.
2
The epigenetics of epithelial-mesenchymal plasticity in cancer.癌症中上皮-间充质可塑性的表观遗传学。
Nat Med. 2013 Nov;19(11):1438-49. doi: 10.1038/nm.3336. Epub 2013 Nov 7.
3
Transcriptional regulation by Polycomb group proteins.多梳蛋白家族通过转录进行调控。
Nat Struct Mol Biol. 2013 Oct;20(10):1147-55. doi: 10.1038/nsmb.2669.
4
Efficient induction of differentiation and growth inhibition in IDH1 mutant glioma cells by the DNMT Inhibitor Decitabine.DNA甲基转移酶抑制剂地西他滨对异柠檬酸脱氢酶1（IDH1）突变型胶质瘤细胞分化的高效诱导及生长抑制作用
Oncotarget. 2013 Oct;4(10):1729-36. doi: 10.18632/oncotarget.1412.
5
5-azacytidine reduces methylation, promotes differentiation and induces tumor regression in a patient-derived IDH1 mutant glioma xenograft.5-氮杂胞苷可降低甲基化水平，促进分化，并在患者来源的异柠檬酸脱氢酶1（IDH1）突变型神经胶质瘤异种移植模型中诱导肿瘤消退。
Oncotarget. 2013 Oct;4(10):1737-47. doi: 10.18632/oncotarget.1408.
6
Induction of sarcomas by mutant IDH2.突变 IDH2 诱导肉瘤。
Genes Dev. 2013 Sep 15;27(18):1986-98. doi: 10.1101/gad.226753.113.
7
Unravelling cancer stem cell potential.解析癌症干细胞潜能。
Nat Rev Cancer. 2013 Oct;13(10):727-38. doi: 10.1038/nrc3597.
8
Tumour heterogeneity and cancer cell plasticity.肿瘤异质性和癌细胞可塑性。
Nature. 2013 Sep 19;501(7467):328-37. doi: 10.1038/nature12624.
9
Oncogenic isocitrate dehydrogenase mutations: mechanisms, models, and clinical opportunities.致癌性异柠檬酸脱氢酶突变：机制、模型和临床机会。
Cancer Discov. 2013 Jul;3(7):730-41. doi: 10.1158/2159-8290.CD-13-0083. Epub 2013 Jun 24.
10
An aberrant transcription factor network essential for Wnt signaling and stem cell maintenance in glioblastoma.异常转录因子网络对胶质母细胞瘤中 Wnt 信号和干细胞维持至关重要。
Cell Rep. 2013 May 30;3(5):1567-79. doi: 10.1016/j.celrep.2013.04.021. Epub 2013 May 23.
Zotero 插件