• 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

丙戊酸联合溶瘤细小病毒 H-1PV 作为治疗宫颈癌和胰腺癌的潜在疗法。

Synergistic combination of valproic acid and oncolytic parvovirus H-1PV as a potential therapy against cervical and pancreatic carcinomas.

机构信息

Infection and Cancer Program, Tumor Virology Division (F010), German Cancer Research Center (DKFZ), Heidelberg, Germany.

出版信息

EMBO Mol Med. 2013 Oct;5(10):1537-55. doi: 10.1002/emmm.201302796. Epub 2013 Sep 17.

DOI:10.1002/emmm.201302796
PMID:24092664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3799578/
Abstract

The rat parvovirus H-1PV has oncolytic and tumour-suppressive properties potentially exploitable in cancer therapy. This possibility is being explored and results are encouraging, but it is necessary to improve the oncotoxicity of the virus. Here we show that this can be achieved by co-treating cancer cells with H-1PV and histone deacetylase inhibitors (HDACIs) such as valproic acid (VPA). We demonstrate that these agents act synergistically to kill a range of human cervical carcinoma and pancreatic carcinoma cell lines by inducing oxidative stress, DNA damage and apoptosis. Strikingly, in rat and mouse xenograft models, H-1PV/VPA co-treatment strongly inhibits tumour growth promoting complete tumour remission in all co-treated animals. At the molecular level, we found acetylation of the parvovirus nonstructural protein NS1 at residues K85 and K257 to modulate NS1-mediated transcription and cytotoxicity, both of which are enhanced by VPA treatment. These results warrant clinical evaluation of H-1PV/VPA co-treatment against cervical and pancreatic ductal carcinomas.

摘要

细小病毒 H-1PV 具有溶瘤和肿瘤抑制特性,可用于癌症治疗。目前正在探索这种可能性,结果令人鼓舞,但有必要提高病毒的致癌毒性。在这里,我们证明通过用 H-1PV 和组蛋白去乙酰化酶抑制剂(HDACIs)(如丙戊酸(VPA))共同处理癌细胞可以实现这一点。我们证明这些药物通过诱导氧化应激、DNA 损伤和细胞凋亡协同作用来杀死一系列人宫颈癌和胰腺癌细胞系。引人注目的是,在大鼠和小鼠异种移植模型中,H-1PV/VPA 共同治疗强烈抑制肿瘤生长,使所有接受共同治疗的动物完全缓解肿瘤。在分子水平上,我们发现细小病毒非结构蛋白 NS1 上残基 K85 和 K257 的乙酰化可调节 NS1 介导的转录和细胞毒性,VPA 处理均可增强这两种作用。这些结果证明了 H-1PV/VPA 共同治疗对宫颈癌和胰腺导管腺癌的临床评估是合理的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/d5da365b3751/emmm0005-1537-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/2407c871ee05/emmm0005-1537-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/17ebffc6c4c7/emmm0005-1537-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/8d2d5414a3b7/emmm0005-1537-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/c9877bcfbaee/emmm0005-1537-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/b969224e2523/emmm0005-1537-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/da74ba36d25c/emmm0005-1537-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/abf692483ab7/emmm0005-1537-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/050aae3605aa/emmm0005-1537-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/6cd617ccefa3/emmm0005-1537-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/d5da365b3751/emmm0005-1537-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/2407c871ee05/emmm0005-1537-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/17ebffc6c4c7/emmm0005-1537-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/8d2d5414a3b7/emmm0005-1537-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/c9877bcfbaee/emmm0005-1537-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/b969224e2523/emmm0005-1537-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/da74ba36d25c/emmm0005-1537-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/abf692483ab7/emmm0005-1537-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/050aae3605aa/emmm0005-1537-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/6cd617ccefa3/emmm0005-1537-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e92/3799578/d5da365b3751/emmm0005-1537-f10.jpg

相似文献

1
Synergistic combination of valproic acid and oncolytic parvovirus H-1PV as a potential therapy against cervical and pancreatic carcinomas.丙戊酸联合溶瘤细小病毒 H-1PV 作为治疗宫颈癌和胰腺癌的潜在疗法。
EMBO Mol Med. 2013 Oct;5(10):1537-55. doi: 10.1002/emmm.201302796. Epub 2013 Sep 17.
2
Improvement of gemcitabine-based therapy of pancreatic carcinoma by means of oncolytic parvovirus H-1PV.通过溶瘤细小病毒H-1PV改善基于吉西他滨的胰腺癌治疗
Clin Cancer Res. 2009 Jan 15;15(2):511-9. doi: 10.1158/1078-0432.CCR-08-1088.
3
Interferon γ improves the vaccination potential of oncolytic parvovirus H-1PV for the treatment of peritoneal carcinomatosis in pancreatic cancer.干扰素 γ 提高溶瘤细小病毒 H-1PV 治疗胰腺癌腹膜转移的疫苗潜力。
Cancer Biol Ther. 2011 Nov 15;12(10):888-95. doi: 10.4161/cbt.12.10.17678.
4
Retargeting of rat parvovirus H-1PV to cancer cells through genetic engineering of the viral capsid.通过对病毒衣壳进行基因工程改造,将大鼠细小病毒 H-1PV 靶向癌细胞。
J Virol. 2012 Apr;86(7):3452-65. doi: 10.1128/JVI.06208-11. Epub 2012 Jan 18.
5
Complementary induction of immunogenic cell death by oncolytic parvovirus H-1PV and gemcitabine in pancreatic cancer.溶瘤细小病毒 H-1PV 和吉西他滨协同诱导胰腺癌免疫原性细胞死亡。
J Virol. 2014 May;88(10):5263-76. doi: 10.1128/JVI.03688-13. Epub 2014 Feb 26.
6
Activation of the human immune system by chemotherapeutic or targeted agents combined with the oncolytic parvovirus H-1.化学治疗或靶向药物联合溶瘤细小病毒 H-1 激活人体免疫系统。
BMC Cancer. 2011 Oct 26;11:464. doi: 10.1186/1471-2407-11-464.
7
Oncolytic H-1 Parvovirus Hijacks Galectin-1 to Enter Cancer Cells.溶瘤 H-1 细小病毒劫持半乳糖凝集素-1 进入癌细胞。
Viruses. 2022 May 11;14(5):1018. doi: 10.3390/v14051018.
8
Preclinical Testing of an Oncolytic Parvovirus in Ewing Sarcoma: Protoparvovirus H-1 Induces Apoptosis and Lytic Infection In Vitro but Fails to Improve Survival In Vivo.成神经细胞瘤瘤病毒的临床前检测:原型细小病毒 H-1 诱导细胞凋亡和溶细胞感染体外,但不能改善体内生存。
Viruses. 2018 Jun 3;10(6):302. doi: 10.3390/v10060302.
9
Oncolytic H-1 parvovirus binds to sialic acid on laminins for cell attachment and entry.溶瘤 H-1 微小病毒通过与层粘连蛋白上的唾液酸结合来实现细胞附着和进入。
Nat Commun. 2021 Jun 22;12(1):3834. doi: 10.1038/s41467-021-24034-7.
10
Combined oncolytic and vaccination activities of parvovirus H-1 in a metastatic tumor model.细小病毒H-1在转移性肿瘤模型中的溶瘤与疫苗接种联合活性
Oncol Rep. 2007 Jun;17(6):1493-9.

引用本文的文献

1
Parvoviruses NS1 oncolytic attributes: mechanistic insights and synergistic anti-tumor therapeutic strategies.细小病毒NS1的溶瘤特性:机制见解与协同抗肿瘤治疗策略
Front Microbiol. 2025 Aug 11;16:1631433. doi: 10.3389/fmicb.2025.1631433. eCollection 2025.
2
Potential Therapeutic Targets for the Treatment of HPV-Associated Malignancies.治疗人乳头瘤病毒相关恶性肿瘤的潜在治疗靶点
Cancers (Basel). 2024 Oct 14;16(20):3474. doi: 10.3390/cancers16203474.
3
Progression of oncolytic virus in liver cancer treatment.溶瘤病毒在肝癌治疗中的进展。

本文引用的文献

1
Intrinsic and extrinsic apoptotic pathway signaling as determinants of histone deacetylase inhibitor antitumor activity.固有和外在凋亡途径信号作为组蛋白去乙酰化酶抑制剂抗肿瘤活性的决定因素。
Adv Cancer Res. 2012;116:165-97. doi: 10.1016/B978-0-12-394387-3.00005-7.
2
HDAC inhibitors: roles of DNA damage and repair.组蛋白去乙酰化酶抑制剂:DNA 损伤与修复的作用。
Adv Cancer Res. 2012;116:87-129. doi: 10.1016/B978-0-12-394387-3.00003-3.
3
Mechanisms of resistance to histone deacetylase inhibitors.组蛋白去乙酰化酶抑制剂耐药机制。
Front Oncol. 2024 Sep 26;14:1446085. doi: 10.3389/fonc.2024.1446085. eCollection 2024.
4
Optimizing Pancreatic Cancer Therapy: The Promise of Immune Stimulatory Oncolytic Viruses.优化胰腺癌治疗:免疫刺激溶瘤病毒的前景。
Int J Mol Sci. 2024 Sep 13;25(18):9912. doi: 10.3390/ijms25189912.
5
Tutorial: design, production and testing of oncolytic viruses for cancer immunotherapy.教程:用于癌症免疫疗法的溶瘤病毒的设计、生产和测试。
Nat Protoc. 2024 Sep;19(9):2540-2570. doi: 10.1038/s41596-024-00985-1. Epub 2024 May 20.
6
Immunotherapeutic Strategies for the Treatment of Glioblastoma: Current Challenges and Future Perspectives.胶质母细胞瘤治疗的免疫治疗策略:当前挑战与未来展望
Cancers (Basel). 2024 Mar 25;16(7):1276. doi: 10.3390/cancers16071276.
7
Developing Oncolytic Viruses for the Treatment of Cervical Cancer.开发溶瘤病毒治疗宫颈癌。
Cells. 2023 Jul 13;12(14):1838. doi: 10.3390/cells12141838.
8
The Emerging Role of Histone Deacetylase Inhibitors in Cervical Cancer Therapy.组蛋白去乙酰化酶抑制剂在宫颈癌治疗中的新兴作用
Cancers (Basel). 2023 Apr 10;15(8):2222. doi: 10.3390/cancers15082222.
9
The role of viruses in cancer development versus cancer therapy: An oncological perspective.病毒在癌症发展与癌症治疗中的作用:肿瘤学视角。
Cancer Med. 2023 May;12(10):11127-11148. doi: 10.1002/cam4.5694. Epub 2023 Mar 7.
10
Design and Characterization of Mutated Variants of the Oncotoxic Parvoviral Protein NS1.设计和鉴定致瘤性细小病毒蛋白 NS1 的突变体变异。
Viruses. 2023 Jan 11;15(1):209. doi: 10.3390/v15010209.
Adv Cancer Res. 2012;116:39-86. doi: 10.1016/B978-0-12-394387-3.00002-1.
4
Generation of an adenovirus-parvovirus chimera with enhanced oncolytic potential.生成具有增强溶瘤潜力的腺病毒-细小病毒嵌合体。
J Virol. 2012 Oct;86(19):10418-31. doi: 10.1128/JVI.00848-12. Epub 2012 Jul 11.
5
Oncolytic virotherapy.溶瘤病毒疗法。
Nat Biotechnol. 2012 Jul 10;30(7):658-70. doi: 10.1038/nbt.2287.
6
High-throughput SNP-based authentication of human cell lines.高通量 SNP 鉴定人源细胞系。
Int J Cancer. 2013 Jan 15;132(2):308-14. doi: 10.1002/ijc.27675. Epub 2012 Jun 28.
7
Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance.新辅助化疗后残留乳腺癌的分析鉴定出 DUSP4 缺陷是耐药的一种机制。
Nat Med. 2012 Jul;18(7):1052-9. doi: 10.1038/nm.2795.
8
Molecular pathways: rodent parvoviruses--mechanisms of oncolysis and prospects for clinical cancer treatment.分子途径:细小病毒--溶瘤机制和临床癌症治疗的前景。
Clin Cancer Res. 2012 Jul 1;18(13):3516-23. doi: 10.1158/1078-0432.CCR-11-2325. Epub 2012 May 7.
9
Phase I/IIa study of intratumoral/intracerebral or intravenous/intracerebral administration of Parvovirus H-1 (ParvOryx) in patients with progressive primary or recurrent glioblastoma multiforme: ParvOryx01 protocol.一项在进展性原发性或复发性多形性胶质母细胞瘤患者中瘤内/颅内或静脉内/颅内给予细小病毒 H-1(ParvOryx)的 I/IIa 期研究:ParvOryx01 方案。
BMC Cancer. 2012 Mar 21;12:99. doi: 10.1186/1471-2407-12-99.
10
The histone deacetylase inhibitor valproic acid lessens NK cell action against oncolytic virus-infected glioblastoma cells by inhibition of STAT5/T-BET signaling and generation of gamma interferon.组蛋白去乙酰化酶抑制剂丙戊酸通过抑制 STAT5/T-BET 信号通路和γ干扰素的产生,减少 NK 细胞对溶瘤病毒感染的神经胶质瘤细胞的作用。
J Virol. 2012 Apr;86(8):4566-77. doi: 10.1128/JVI.05545-11. Epub 2012 Feb 8.