• 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

丝裂原活化蛋白激酶（MAPK）信号传导调节化学免疫疗法的疗效。

MAPK signaling regulates the efficacy of chemoimmunotherapy.

作者信息

Ghiringhelli François

机构信息

Leclerc, Equipe Labellisée Ligue Contre le CancerCancer Biology Transfer Platform, Centre Georges-François, Dijon, France.

Centre de Recherche INSERM LNC-UMR1231, Dijon, France.

出版信息

Mol Cell Oncol. 2022 Apr 27;9(1):2054652. doi: 10.1080/23723556.2022.2054652. eCollection 2022.

DOI:10.1080/23723556.2022.2054652
PMID:35529902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9067517/
Abstract

Resistance to chemoimmunotherapy is a major issue for cancer care. We recently unravelled the role of mitogen-activated protein kinase (MAPK) to limit the antitumor efficacy of such combination. Inhibitor of MAPK pathway using mitogen-activated protein kinase (MEK) inhibitor in combination with chemotherapy triggers mitophagy of cancer cells, which induces the release of mitochondrial DNA that interact with Toll Like receptor 9 (TLR9) to promote the production of the chemokine CXCL10. CXCL10 could then turn cold tumor into hot tumor, thus leading to improve efficacy of chemoimmunotherapy.

摘要

对化学免疫疗法的耐药性是癌症治疗中的一个主要问题。我们最近揭示了丝裂原活化蛋白激酶（MAPK）在限制这种联合疗法抗肿瘤疗效方面的作用。使用丝裂原活化蛋白激酶（MEK）抑制剂抑制MAPK通路并联合化疗会引发癌细胞的线粒体自噬，这会诱导线粒体DNA的释放，其与Toll样受体9（TLR9）相互作用以促进趋化因子CXCL10的产生。然后，CXCL10可将冷肿瘤转变为热肿瘤，从而提高化学免疫疗法的疗效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aacf/9067517/aa8bb9b712ed/KMCO_A_2054652_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aacf/9067517/aa8bb9b712ed/KMCO_A_2054652_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aacf/9067517/aa8bb9b712ed/KMCO_A_2054652_F0001_OC.jpg

相似文献

1
MAPK signaling regulates the efficacy of chemoimmunotherapy.丝裂原活化蛋白激酶（MAPK）信号传导调节化学免疫疗法的疗效。
Mol Cell Oncol. 2022 Apr 27;9(1):2054652. doi: 10.1080/23723556.2022.2054652. eCollection 2022.
2
MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells.MEK 抑制通过诱导癌细胞中的 CXCL10 克服化疗免疫治疗耐药性。
Cancer Cell. 2022 Feb 14;40(2):136-152.e12. doi: 10.1016/j.ccell.2021.12.009. Epub 2022 Jan 19.
3
Mitophagy: a new actor in the efficacy of chemo-immunotherapy.自噬：化疗免疫治疗疗效的新因素。
Autophagy. 2022 Dec;18(12):3033-3034. doi: 10.1080/15548627.2022.2069439. Epub 2022 May 9.
4
MEK inhibition invigorates chemoimmunotherapy by tumor mitophagy-induced CXCL10 expression.MEK 抑制通过肿瘤细胞噬作用诱导的 CXCL10 表达增强化疗免疫治疗。
Cell Rep Med. 2022 Jan 18;3(1):100506. doi: 10.1016/j.xcrm.2021.100506.
5
The role of MAPK in Kupffer cell toll-like receptor (TLR) 2-, TLR4-, and TLR9-mediated signaling following trauma-hemorrhage.丝裂原活化蛋白激酶（MAPK）在创伤性出血后库普弗细胞Toll样受体（TLR）2、TLR4和TLR9介导的信号传导中的作用。
J Cell Physiol. 2007 Mar;210(3):667-75. doi: 10.1002/jcp.20860.
6
Pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase/MAPK cascade interact synergistically with UCN-01 to induce mitochondrial dysfunction and apoptosis in human leukemia cells.丝裂原活化蛋白激酶（MAPK）激酶/MAPK级联反应的药理学抑制剂与UCN-01协同作用，诱导人白血病细胞的线粒体功能障碍和凋亡。
Cancer Res. 2001 Jul 1;61(13):5106-15.
7
Toll-like receptor 9 signaling promotes autophagy and apoptosis via divergent functions of the p38/JNK pathway in human salivary gland cells.Toll 样受体 9 信号通路通过 p38/JNK 通路的不同功能促进人唾液腺细胞自噬和凋亡。
Exp Cell Res. 2019 Feb 15;375(2):51-59. doi: 10.1016/j.yexcr.2018.12.027. Epub 2019 Jan 3.
8
Prolactin enhances interferon-gamma-induced production of CXC ligand 9 (CXCL9), CXCL10, and CXCL11 in human keratinocytes.催乳素可增强干扰素-γ诱导人角质形成细胞产生CXC配体9（CXCL9）、CXCL10和CXCL11。
Endocrinology. 2007 May;148(5):2317-25. doi: 10.1210/en.2006-1639. Epub 2007 Jan 25.
9
Key roles of EMT for adaptive resistance to MEK inhibitor in KRAS mutant lung cancer.上皮-间质转化（EMT）在KRAS突变型肺癌对MEK抑制剂适应性耐药中的关键作用
Small GTPases. 2017 Jul 3;8(3):172-176. doi: 10.1080/21541248.2016.1210369. Epub 2016 Jul 8.
10
Collaborative action of NF-kappaB and p38 MAPK is involved in CpG DNA-induced IFN-alpha and chemokine production in human plasmacytoid dendritic cells.核因子-κB（NF-κB）与p38丝裂原活化蛋白激酶（p38 MAPK）的协同作用参与了人浆细胞样树突状细胞中CpG DNA诱导的Ⅰ型干扰素（IFN-α）和趋化因子的产生。
J Immunol. 2006 Oct 1;177(7):4841-52. doi: 10.4049/jimmunol.177.7.4841.

本文引用的文献

1
MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells.MEK 抑制通过诱导癌细胞中的 CXCL10 克服化疗免疫治疗耐药性。
Cancer Cell. 2022 Feb 14;40(2):136-152.e12. doi: 10.1016/j.ccell.2021.12.009. Epub 2022 Jan 19.
2
Short-term treatment with multi-drug regimens combining BRAF/MEK-targeted therapy and immunotherapy results in durable responses in -mutated melanoma.联合 BRAF/MEK 靶向治疗和免疫治疗的多药物方案短期治疗可导致 - 突变黑色素瘤获得持久缓解。
Oncoimmunology. 2021 Nov 6;10(1):1992880. doi: 10.1080/2162402X.2021.1992880. eCollection 2021.
3
Immunomodulation by targeted anticancer agents.
靶向抗癌药物的免疫调节作用。
Cancer Cell. 2021 Mar 8;39(3):310-345. doi: 10.1016/j.ccell.2020.11.009. Epub 2020 Dec 17.
4
Evolutionary divergence of HLA class I genotype impacts efficacy of cancer immunotherapy.HLA 类 I 基因型的进化分歧影响癌症免疫疗法的疗效。
Nat Med. 2019 Nov;25(11):1715-1720. doi: 10.1038/s41591-019-0639-4. Epub 2019 Nov 7.
5
The evolving landscape of biomarkers for checkpoint inhibitor immunotherapy.不断发展的免疫检查点抑制剂治疗生物标志物。
Nat Rev Cancer. 2019 Mar;19(3):133-150. doi: 10.1038/s41568-019-0116-x.
6
Pembrolizumab plus Chemotherapy in Metastatic Non-Small-Cell Lung Cancer.帕博利珠单抗联合化疗治疗转移性非小细胞肺癌。
N Engl J Med. 2018 May 31;378(22):2078-2092. doi: 10.1056/NEJMoa1801005. Epub 2018 Apr 16.
7
Cancer immunology. Mutational landscape determines sensitivity to PD-1 blockade in non-small cell lung cancer.癌症免疫学。突变图谱决定非小细胞肺癌对程序性死亡受体1（PD-1）阻断治疗的敏感性。
Science. 2015 Apr 3;348(6230):124-8. doi: 10.1126/science.aaa1348. Epub 2015 Mar 12.
8
Activation of the NLRP3 inflammasome in dendritic cells induces IL-1beta-dependent adaptive immunity against tumors.树突状细胞中NLRP3炎性小体的激活诱导针对肿瘤的白细胞介素-1β依赖性适应性免疫。
Nat Med. 2009 Oct;15(10):1170-8. doi: 10.1038/nm.2028. Epub 2009 Sep 20.
9
Toll-like receptor 4-dependent contribution of the immune system to anticancer chemotherapy and radiotherapy.免疫系统通过Toll样受体4对癌症化疗和放疗的作用
Nat Med. 2007 Sep;13(9):1050-9. doi: 10.1038/nm1622. Epub 2007 Aug 19.
10
Calreticulin exposure dictates the immunogenicity of cancer cell death.钙网蛋白的暴露决定了癌细胞死亡的免疫原性。
Nat Med. 2007 Jan;13(1):54-61. doi: 10.1038/nm1523. Epub 2006 Dec 24.