• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

常染色质组蛋白赖氨酸甲基转移酶2抑制增强卡非佐米敏感性并克服多发性骨髓瘤细胞系中的耐药性。

Euchromatic Histone Lysine Methyltransferase 2 Inhibition Enhances Carfilzomib Sensitivity and Overcomes Drug Resistance in Multiple Myeloma Cell Lines.

作者信息

Mereu Elisabetta, Abbo Damiano, Paradzik Tina, Cumerlato Michela, Bandini Cecilia, Labrador Maria, Maccagno Monica, Ronchetti Domenica, Manicardi Veronica, Neri Antonino, Piva Roberto

机构信息

Department of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.

Department of Physical Chemistry, Rudjer Boskovic Insitute, 10000 Zagreb, Croatia.

出版信息

Cancers (Basel). 2023 Apr 7;15(8):2199. doi: 10.3390/cancers15082199.

DOI:10.3390/cancers15082199
PMID:37190128
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10137151/
Abstract

Proteasome inhibitors (PIs) are extensively used for the therapy of multiple myeloma. However, patients continuously relapse or are intrinsically resistant to this class of drugs. In addition, adverse toxic effects such as peripheral neuropathy and cardiotoxicity could arise. Here, to identify compounds that can increase the efficacy of PIs, we performed a functional screening using a library of small-molecule inhibitors covering key signaling pathways. Among the best synthetic lethal interactions, the euchromatic histone-lysine N-methyltransferase 2 (EHMT2) inhibitor UNC0642 displayed a cooperative effect with carfilzomib (CFZ) in numerous multiple myeloma (MM) cell lines, including drug-resistant models. In MM patients, EHMT2 expression correlated to worse overall and progression-free survival. Moreover, EHMT2 levels were significantly increased in bortezomib-resistant patients. We demonstrated that CFZ/UNC0642 combination exhibited a favorable cytotoxicity profile toward peripheral blood mononuclear cells and bone-marrow-derived stromal cells. To exclude off-target effects, we proved that UNC0642 treatment reduces EHMT2-related molecular markers and that an alternative EHMT2 inhibitor recapitulated the synergistic activity with CFZ. Finally, we showed that the combinatorial treatment significantly perturbs autophagy and the DNA damage repair pathways, suggesting a multi-layered mechanism of action. Overall, the present study demonstrates that EHMT2 inhibition could provide a valuable strategy to enhance PI sensitivity and overcome drug resistance in MM patients.

摘要

蛋白酶体抑制剂(PIs)被广泛用于治疗多发性骨髓瘤。然而,患者会持续复发或对这类药物存在内在抗性。此外,还可能出现外周神经病变和心脏毒性等不良毒性作用。在此,为了鉴定能够提高PIs疗效的化合物,我们使用涵盖关键信号通路的小分子抑制剂文库进行了功能筛选。在最佳的合成致死相互作用中,常染色质组蛋白赖氨酸N-甲基转移酶2(EHMT2)抑制剂UNC0642在众多多发性骨髓瘤(MM)细胞系(包括耐药模型)中与卡非佐米(CFZ)表现出协同效应。在MM患者中,EHMT2表达与较差的总生存期和无进展生存期相关。此外,硼替佐米耐药患者的EHMT2水平显著升高。我们证明CFZ/UNC0642组合对外周血单个核细胞和骨髓来源的基质细胞表现出良好的细胞毒性特征。为了排除脱靶效应,我们证明UNC0642处理可降低与EHMT2相关的分子标志物,并且另一种EHMT2抑制剂重现了与CFZ的协同活性。最后,我们表明联合治疗显著扰乱自噬和DNA损伤修复途径,提示其具有多层作用机制。总体而言,本研究表明抑制EHMT2可为提高MM患者对PI的敏感性和克服耐药性提供有价值的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/5e5f1c36a664/cancers-15-02199-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/90d46e9bb004/cancers-15-02199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/7453074417dc/cancers-15-02199-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/93e2fb12784e/cancers-15-02199-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/00265decaa6f/cancers-15-02199-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/b18d19ffef0c/cancers-15-02199-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/5e5f1c36a664/cancers-15-02199-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/90d46e9bb004/cancers-15-02199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/7453074417dc/cancers-15-02199-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/93e2fb12784e/cancers-15-02199-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/00265decaa6f/cancers-15-02199-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/b18d19ffef0c/cancers-15-02199-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba5/10137151/5e5f1c36a664/cancers-15-02199-g006.jpg

相似文献

1
Euchromatic Histone Lysine Methyltransferase 2 Inhibition Enhances Carfilzomib Sensitivity and Overcomes Drug Resistance in Multiple Myeloma Cell Lines.常染色质组蛋白赖氨酸甲基转移酶2抑制增强卡非佐米敏感性并克服多发性骨髓瘤细胞系中的耐药性。
Cancers (Basel). 2023 Apr 7;15(8):2199. doi: 10.3390/cancers15082199.
2
Lysin (K)-specific demethylase 1 inhibition enhances proteasome inhibitor response and overcomes drug resistance in multiple myeloma.赖氨酰(K)特异性去甲基化酶1抑制可增强蛋白酶体抑制剂反应并克服多发性骨髓瘤中的耐药性。
Exp Hematol Oncol. 2023 Aug 10;12(1):71. doi: 10.1186/s40164-023-00434-x.
3
IDH2 inhibition enhances proteasome inhibitor responsiveness in hematological malignancies.异柠檬酸脱氢酶 2 抑制增强血液系统恶性肿瘤对蛋白酶体抑制剂的反应性。
Blood. 2019 Jan 10;133(2):156-167. doi: 10.1182/blood-2018-05-850826. Epub 2018 Nov 19.
4
Bortezomib- and carfilzomib-resistant myeloma cells show increased activity of all three arms of the unfolded protein response.硼替佐米和卡非佐米耐药的骨髓瘤细胞显示出未折叠蛋白反应的所有三个分支的活性增加。
Am J Cancer Res. 2022 Jul 15;12(7):3280-3293. eCollection 2022.
5
XPO1 inhibitor combination therapy with bortezomib or carfilzomib induces nuclear localization of IκBα and overcomes acquired proteasome inhibitor resistance in human multiple myeloma.XPO1抑制剂与硼替佐米或卡非佐米联合治疗可诱导IκBα的核定位,并克服人多发性骨髓瘤中获得性蛋白酶体抑制剂耐药性。
Oncotarget. 2016 Nov 29;7(48):78896-78909. doi: 10.18632/oncotarget.12969.
6
TOP2A expression predicts responsiveness to carfilzomib in myeloma and informs novel combinatorial strategies for enhanced proteasome inhibitor cell killing.TOP2A 表达预测多发性骨髓瘤对卡非佐米的反应性,并为增强蛋白酶体抑制剂细胞杀伤提供新的组合策略。
Leuk Lymphoma. 2021 Feb;62(2):337-347. doi: 10.1080/10428194.2020.1832659. Epub 2020 Oct 31.
7
Histone-lysine methyltransferase EHMT2 is involved in proliferation, apoptosis, cell invasion, and DNA methylation of human neuroblastoma cells.组蛋白赖氨酸甲基转移酶 EHMT2 参与人神经母细胞瘤细胞的增殖、凋亡、细胞侵袭和 DNA 甲基化。
Anticancer Drugs. 2013 Jun;24(5):484-93. doi: 10.1097/CAD.0b013e32835ffdbb.
8
The novel β2-selective proteasome inhibitor LU-102 synergizes with bortezomib and carfilzomib to overcome proteasome inhibitor resistance of myeloma cells.新型β2选择性蛋白酶体抑制剂LU-102与硼替佐米和卡非佐米协同作用,克服骨髓瘤细胞对蛋白酶体抑制剂的耐药性。
Haematologica. 2015 Oct;100(10):1350-60. doi: 10.3324/haematol.2014.109421. Epub 2015 Jun 11.
9
Nelfinavir augments proteasome inhibition by bortezomib in myeloma cells and overcomes bortezomib and carfilzomib resistance.奈非那韦增强硼替佐米在骨髓瘤细胞中的蛋白酶体抑制作用,并克服硼替佐米和卡非佐米耐药性。
Blood Cancer J. 2013 Mar 1;3(3):e103. doi: 10.1038/bcj.2013.2.
10
The novel β2-selective proteasome inhibitor LU-102 decreases phosphorylation of I kappa B and induces highly synergistic cytotoxicity in combination with ibrutinib in multiple myeloma cells.新型β2选择性蛋白酶体抑制剂LU-102可降低IκB的磷酸化水平,并与依鲁替尼联合使用时在多发性骨髓瘤细胞中诱导高度协同的细胞毒性。
Cancer Chemother Pharmacol. 2015 Aug;76(2):383-96. doi: 10.1007/s00280-015-2801-0. Epub 2015 Jun 23.

引用本文的文献

1
Atypical R-loops in cancer: decoding molecular chaos for therapeutic gain.癌症中的非典型R环:破解分子混乱以实现治疗效益。
J Transl Med. 2025 Aug 14;23(1):912. doi: 10.1186/s12967-025-06929-x.
2
Ginsenoside Rg1 inhibits multiple myeloma and overcomes bortezomib resistance through AMPK-mTOR pathway.人参皂苷Rg1通过AMPK-mTOR途径抑制多发性骨髓瘤并克服硼替佐米耐药性。
Heliyon. 2024 Jul 1;10(13):e33935. doi: 10.1016/j.heliyon.2024.e33935. eCollection 2024 Jul 15.
3
Combinatorial strategies targeting NEAT1 and AURKA as new potential therapeutic options for multiple myeloma.

本文引用的文献

1
Expression levels of NONO, a nuclear protein primarily involved in paraspeckles function, are associated with several deregulated molecular pathways and poor clinical outcome in multiple myeloma.NONO是一种主要参与副斑点功能的核蛋白,其表达水平与多种骨髓瘤中几条失调的分子途径及不良临床预后相关。
Discov Oncol. 2022 Nov 11;13(1):124. doi: 10.1007/s12672-022-00582-2.
2
Protocol for generation of 3D bone marrow surrogate microenvironments in a rotary cell culture system.旋转细胞培养系统中 3D 骨髓替代微环境的生成方案。
STAR Protoc. 2022 Aug 10;3(3):101601. doi: 10.1016/j.xpro.2022.101601. eCollection 2022 Sep 16.
3
靶向NEAT1和AURKA的联合策略作为多发性骨髓瘤新的潜在治疗选择。
Haematologica. 2024 Dec 1;109(12):4040-4055. doi: 10.3324/haematol.2024.285470.
4
G9a in Cancer: Mechanisms, Therapeutic Advancements, and Clinical Implications.G9a在癌症中的作用:机制、治疗进展及临床意义
Cancers (Basel). 2024 Jun 8;16(12):2175. doi: 10.3390/cancers16122175.
5
Factors determining the sensitivity to proteasome inhibitors of multiple myeloma cells.决定多发性骨髓瘤细胞对蛋白酶体抑制剂敏感性的因素。
Front Pharmacol. 2024 Mar 4;15:1351565. doi: 10.3389/fphar.2024.1351565. eCollection 2024.
6
Gene signatures to therapeutics: Assessing the potential of ivermectin against t(4;14) multiple myeloma.基因特征与治疗:评估伊维菌素对t(4;14)多发性骨髓瘤的治疗潜力。
World J Clin Oncol. 2024 Jan 24;15(1):115-129. doi: 10.5306/wjco.v15.i1.115.
7
Understanding DNA Epigenetics by Means of Raman/SERS Analysis for Cancer Detection.通过拉曼/ SERS 分析理解 DNA 表观遗传学以用于癌症检测。
Biosensors (Basel). 2024 Jan 12;14(1):41. doi: 10.3390/bios14010041.
8
Lysin (K)-specific demethylase 1 inhibition enhances proteasome inhibitor response and overcomes drug resistance in multiple myeloma.赖氨酰(K)特异性去甲基化酶1抑制可增强蛋白酶体抑制剂反应并克服多发性骨髓瘤中的耐药性。
Exp Hematol Oncol. 2023 Aug 10;12(1):71. doi: 10.1186/s40164-023-00434-x.
Lysine methyltransferase inhibitors: where we are now.
赖氨酸甲基转移酶抑制剂:我们目前的进展
RSC Chem Biol. 2021 Dec 13;3(4):359-406. doi: 10.1039/d1cb00196e. eCollection 2022 Apr 6.
4
Dual Inhibition of H3K9me2 and H3K27me3 Promotes Tumor Cell Senescence without Triggering the Secretion of SASP.对H3K9me2和H3K27me3的双重抑制促进肿瘤细胞衰老而不引发衰老相关分泌表型的分泌。
Int J Mol Sci. 2022 Apr 1;23(7):3911. doi: 10.3390/ijms23073911.
5
EHMT1/EHMT2 in EMT, cancer stemness and drug resistance: emerging evidence and mechanisms.EHMT1/EHMT2 在 EMT、癌症干性和耐药性中的作用:新出现的证据和机制。
FEBS J. 2022 Mar;289(5):1329-1351. doi: 10.1111/febs.16334. Epub 2022 Jan 8.
6
EHMT2 (G9a) activation in mantle cell lymphoma and its associated DNA methylation and gene expression.EHMT2(G9a)在套细胞淋巴瘤中的激活及其相关的 DNA 甲基化和基因表达。
Cancer Biol Med. 2021 Oct 12;19(6):836-49. doi: 10.20892/j.issn.2095-3941.2020.0371.
7
G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death.在多发性骨髓瘤中靶向 G9a/GLP 可促进自噬相关的细胞凋亡,并增强蛋白酶体抑制剂介导的细胞死亡。
Blood Adv. 2021 May 11;5(9):2325-2338. doi: 10.1182/bloodadvances.2020003217.
8
The Landscape of Signaling Pathways and Proteasome Inhibitors Combinations in Multiple Myeloma.多发性骨髓瘤中信号通路与蛋白酶体抑制剂联合应用的格局
Cancers (Basel). 2021 Mar 11;13(6):1235. doi: 10.3390/cancers13061235.
9
Multiple myeloma.多发性骨髓瘤。
Lancet. 2021 Jan 30;397(10272):410-427. doi: 10.1016/S0140-6736(21)00135-5.
10
Dual EZH2 and G9a inhibition suppresses multiple myeloma cell proliferation by regulating the interferon signal and IRF4-MYC axis.EZH2和G9a双重抑制通过调节干扰素信号和IRF4-MYC轴抑制多发性骨髓瘤细胞增殖。
Cell Death Discov. 2021 Jan 12;7(1):7. doi: 10.1038/s41420-020-00400-0.