AbstractNeurofibromatosis type 2 (NF2) is a rare disorder that causes vestibular schwannomas (VS), meningiomas and ependymomas. To date, there is no FDA approved drug-based treatment for NF2. We have previously identified that BET inhibition can selectively reduce growth of the NF2-null schwannoma and Schwann cells in vitro and tumorigenesis in vivo and, separately, reported that inhibition of Focal Adhesion Kinase 1 (FAK1) via crizotinib has antiproliferative effects in NF2-null Schwann cells.

摘要2型神经纤维瘤病（NF2）是一种罕见的疾病，可引起前庭神经鞘瘤（VS），脑膜瘤和室管膜瘤。迄今为止，尚无FDA批准的基于药物的NF2治疗方法。我们先前已经确定BET抑制可以选择性地减少体外NF2无效神经鞘瘤和雪旺氏细胞的生长以及体内肿瘤发生，并且分别报道了通过克唑替尼抑制粘着斑激酶1（FAK1）对NF2无效的雪旺氏细胞具有抗增殖作用。

The current study was aimed at determining whether combined BET and FAK inhibition can synergize and to identify the mechanisms of action. A panel of normal and NF2-null Schwann and schwannoma cell lines were used to characterize the effects of combined BET and FAK inhibition in vitro and in vivo using pharmacological and genetic approaches.

目前的研究旨在确定BET和FAK联合抑制是否可以协同作用，并确定其作用机制。使用一组正常和NF2无效的神经鞘瘤和神经鞘瘤细胞系，使用药理学和遗传学方法在体外和体内表征BET和FAK联合抑制的作用。

The mechanism of action was explored by chromatin immunoprecipitation, ChIP-PCR, western blotting, and functional approaches. We find that combined BET and FAK inhibition are synergistic and inhibit the proliferation of NF2-null schwannoma and Schwann cell lines in vitro and in vivo, by arresting cells in the G1/S and G2/M phases of the cell cycle.

通过染色质免疫沉淀，ChIP-PCR，蛋白质印迹和功能方法探索了作用机制。我们发现BET和FAK联合抑制具有协同作用，并通过将细胞阻滞在细胞周期的G1/S和G2/M期，在体外和体内抑制NF2无效神经鞘瘤和雪旺氏细胞系的增殖。

Further, we identify the mechanism of action through the downregulation of FAK1 transcription by BET inhibition, which potentiates inhibition of FAK by 100-fold. Our findings suggest that combined targeting of BET and FAK1 may offer a potential therapeutic option for the treatment of NF2-related schwannomas..

此外，我们通过BET抑制下调FAK1转录来确定作用机制，这将FAK的抑制作用增强了100倍。我们的研究结果表明，BET和FAK1的联合靶向可能为治疗NF2相关神经鞘瘤提供潜在的治疗选择。。

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Fig. 1: Impact of BET and FAK inhibition on NF2-null Schwann cell growth.Fig. 2: Combined BET and FAK inhibition synergize in inhibition of NF2-null Schwann cell growth.Fig. 3: Combined BET and FAK inhibition arrest NF2-null Schwann cells in the G1/S and G2/M phases of the cell cycle.Fig. 4: Combined BET and FAK inhibition synergize in inhibition of NF2-null Schwann tumor growth.Fig.

图1:BET和FAK抑制对NF2无效雪旺氏细胞生长的影响。图2:BET和FAK联合抑制协同抑制NF2无效的雪旺细胞生长。图3:BET和FAK联合抑制将NF2-null雪旺氏细胞阻滞在细胞周期的G1/S和G2/M期。图4:BET和FAK联合抑制协同抑制NF2无效的雪旺氏肿瘤生长。图。

5: BET inhibition negatively impacts the expression of FAK1..

5： BET抑制对FAK1的表达产生负面影响。。

Data availability

数据可用性

The ChIP-seq data were originally reported in [11] and are available from the Gene Expression Omnibus under accession number GSE167560. All other raw data is available upon request from the corresponding author.

ChIP-seq数据最初在文献[11]中报道，可从Gene Expression Omnibus获得，登录号为GSE167560。所有其他原始数据均可根据通讯作者的要求获得。

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Download referencesAcknowledgementsThe work was supported by NS117926 (NINDS/NIH) to JK. MK is supported by the NIH NCI/NIGMS grant R01CA233661 and the NIH NIGMS Center for Pediatric Research 5P20GM103620. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.Author informationAuthors and AffiliationsDepartment of Molecular Oncology and H.

下载参考文献致谢这项工作得到了NS117926（NINDS/NIH）对JK的支持。MK得到了NIH NCI/NIGMS拨款R01CA233661和NIH NIGMS儿科研究中心5P20GM103620的支持。内容完全由作者负责，不一定代表美国国立卫生研究院的官方观点。作者信息作者和附属机构分子肿瘤学系和H。

Lee Moffitt Cancer Center, Tampa, FL, USAMaria A. González-Rodriguez, Scott Troutman, Daniel K. Lester, Matthew Grove & Joseph L. KissilDrug Discovery, H. Lee Moffitt Cancer Center, Tampa, FL, USASimon Bayle & Derek DuckettGenetics and Genomics Group, Sanford Research, Sioux Falls, SD, USAMichael S.

Lee Moffitt癌症中心，佛罗里达州坦帕，USAMaria A.González Rodriguez，Scott Troutman，Daniel K.Lester，Matthew Grove＆Joseph L.KissilDrug Discovery，H.Lee Moffitt癌症中心，佛罗里达州坦帕，USASimon Bayle＆Derek DuckettGenetics and Genomics Group，Sanford Research，Sioux Falls，SD，USAMAChael S。

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PubMed Google ScholarContributionsConceptualization- MAG-R and JLK. Investigation - MAG-R, ST, SB, MSK, DL, and MG. Analysis - MAG-R, SB, ST, MSK, DD, DL, MG and JLK. Writing MAG-R, and JLK. Editing - MAG-R, SB., ST, MSK, DD and JLK. Funding acquisition– JLK.Corresponding authorCorrespondence to.

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Competing interests

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The authors declare no conflict of interest exists. JLK serves as a member of the Scientific Advisory Board for Mulberry Therapeutics.

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道德批准和同意参与

The authors declare that all methods were performed in accordance with all relevant guidelines and regulations. All animal experiments complied with NIH guidelines and were approved by the Moffitt Cancer Center IACUC under protocol IS00008425. As this study did not include any patient material there was no need for informed consent..

作者声明，所有方法均按照所有相关指南和法规进行。所有动物实验均符合NIH指南，并由Moffitt癌症中心IACUC根据协议IS00008425批准。由于这项研究不包括任何患者材料，因此不需要知情同意。。

Additional informationPublisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.Supplementary informationSupplemental MaterialRights and permissionsSpringer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.Reprints and permissionsAbout this articleCite this articleGonzález-Rodriguez, M.A., Troutman, S., Bayle, S.

Additional informationPublisher的注释Springer Nature在已发布的地图和机构隶属关系中的管辖权主张方面保持中立。补充信息补充材料权利和许可Pringer Nature或其许可方（例如协会或其他合作伙伴）根据与作者或其他权利持有人的出版协议对本文拥有专有权；本文接受稿件版本的作者自行存档仅受此类出版协议和适用法律的条款管辖。转载和许可本文引用本文González Rodriguez，M.A.，Troutman，S.，Bayle，S。

et al. Synergistic effects of combined BET and FAK inhibition against Vestibular Schwannomas in NF2-related Schwannomatosis..

BET和FAK联合抑制对NF2相关神经鞘瘤病中前庭神经鞘瘤的协同作用。。

Oncogene (2024). https://doi.org/10.1038/s41388-024-03144-8Download citationReceived: 15 May 2024Revised: 14 August 2024Accepted: 22 August 2024Published: 29 August 2024DOI: https://doi.org/10.1038/s41388-024-03144-8Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

癌基因（2024）。https://doi.org/10.1038/s41388-024-03144-8Download引文收到日期：2024年5月15日修订日期：2024年8月14日接受日期：2024年8月22日发布日期：2024年8月29日OI：https://doi.org/10.1038/s41388-024-03144-8Share本文与您共享以下链接的任何人都可以阅读此内容：获取可共享链接对不起，本文目前没有可共享的链接。复制到剪贴板。

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