文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期,新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
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
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
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 @ 2025

瘤内 TLR4 激动剂治疗增强了器官对脑内定植癌细胞的防御能力。

Intralesional TLR4 agonist treatment strengthens the organ defense against colonizing cancer cells in the brain.

机构信息

Department of Internal Medicine III, Hematology and Medical Oncology, University Hospital Regensburg, 93053, Regensburg, Germany.

Department of Hematology and Medical Oncology, University Medical Center Göttingen, 37075, Göttingen, Germany.

出版信息

Oncogene. 2022 Nov;41(46):5008-5019. doi: 10.1038/s41388-022-02496-3. Epub 2022 Oct 12.


DOI:10.1038/s41388-022-02496-3
PMID:36224342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9652147/
Abstract

Brain metastasis in breast cancer remains difficult to treat and its incidence is increasing. Therefore, the development of new therapies is of utmost clinical relevance. Recently, toll-like receptor (TLR) 4 was correlated with IL6 expression and poor prognosis in 1 215 breast cancer primaries. In contrast, we demonstrated that TLR4 stimulation reduces microglia-assisted breast cancer cell invasion. However, the expression, prognostic value, or therapeutic potential of TLR signaling in breast cancer brain metastasis have not been investigated. We thus tested the prognostic value of various TLRs in two brain-metastasis gene sets. Furthermore, we investigated different TLR agonists, as well as MyD88 and TRIF-deficient microenvironments in organotypic brain-slice ex vivo co-cultures and in vivo colonization experiments. These experiments underline the ambiguous roles of TLR4, its adapter MyD88, and the target nitric oxide (NO) during brain colonization. Moreover, analysis of the gene expression datasets of breast cancer brain metastasis patients revealed associations of TLR1 and IL6 with poor overall survival. Finally, our finding that a single LPS application at the onset of colonization shapes the later microglia/macrophage reaction at the macro-metastasis brain-parenchyma interface (MMPI) and reduces metastatic infiltration into the brain parenchyma may prove useful in immunotherapeutic considerations.

摘要

乳腺癌脑转移仍然难以治疗,其发病率正在增加。因此,开发新的治疗方法具有非常重要的临床意义。最近,TLR4 与 IL6 表达和 1215 例乳腺癌原发灶的不良预后相关。相比之下,我们证明 TLR4 刺激可减少小胶质细胞辅助的乳腺癌细胞侵袭。然而,TLR 信号在乳腺癌脑转移中的表达、预后价值或治疗潜力尚未得到研究。因此,我们在两个脑转移基因集中测试了各种 TLR 的预后价值。此外,我们还研究了不同的 TLR 激动剂,以及在器官型脑切片体外共培养和体内定植实验中 MyD88 和 TRIF 缺陷的微环境。这些实验强调了 TLR4、其衔接子 MyD88 和靶标一氧化氮(NO)在脑定植过程中的作用。此外,对乳腺癌脑转移患者的基因表达数据集进行分析,发现 TLR1 和 IL6 与总体生存不良相关。最后,我们发现,在定植开始时单次 LPS 应用可塑造宏观转移脑实质界面(MMPI)处的小胶质细胞/巨噬细胞反应,并减少转移浸润到脑实质,这可能对免疫治疗的考虑有用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/a67844d3e844/41388_2022_2496_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/b87f508d059a/41388_2022_2496_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/0e095c35c2e5/41388_2022_2496_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/0a7c23b441a3/41388_2022_2496_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/aec19c868c29/41388_2022_2496_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/b52af62039e1/41388_2022_2496_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/a67844d3e844/41388_2022_2496_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/b87f508d059a/41388_2022_2496_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/0e095c35c2e5/41388_2022_2496_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/0a7c23b441a3/41388_2022_2496_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/aec19c868c29/41388_2022_2496_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/b52af62039e1/41388_2022_2496_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c22/9652147/a67844d3e844/41388_2022_2496_Fig6_HTML.jpg

相似文献

[1]
Intralesional TLR4 agonist treatment strengthens the organ defense against colonizing cancer cells in the brain.

Oncogene. 2022-11

[2]
The IRAK4 scaffold integrates TLR4-driven TRIF and MYD88 signaling pathways.

Cell Rep. 2022-8-16

[3]
Signaling of apoptosis through TLRs critically involves toll/IL-1 receptor domain-containing adapter inducing IFN-beta, but not MyD88, in bacteria-infected murine macrophages.

J Immunol. 2004-9-1

[4]
Endotoxin tolerance dysregulates MyD88- and Toll/IL-1R domain-containing adapter inducing IFN-beta-dependent pathways and increases expression of negative regulators of TLR signaling.

J Leukoc Biol. 2009-10

[5]
TLR4/MyD88 signaling determines the metastatic potential of breast cancer cells.

Mol Med Rep. 2018-7-26

[6]
Recipient Toll-like receptors contribute to chronic graft dysfunction by both MyD88- and TRIF-dependent signaling.

Dis Model Mech. 2009-12-28

[7]
Dual regulation of osteopontin production by TLR stimulation in dendritic cells.

J Leukoc Biol. 2013-4-22

[8]
Biologically active 1,25-dihydroxyvitamin D3 protects against experimental sepsis by negatively regulating the Toll-like receptor 4/myeloid differentiation primary response gene 88/Toll-IL-1 resistance-domain-containing adapter-inducing interferon-β signaling pathway.

Int J Mol Med. 2019-7-5

[9]
Melatonin attenuates the TLR4-mediated inflammatory response through MyD88- and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer.

BMC Cancer. 2015-2-6

[10]
Dominant role of the MyD88-dependent signaling pathway in mediating early endotoxin-induced murine ileus.

Am J Physiol Gastrointest Liver Physiol. 2010-5-27

引用本文的文献

[1]
Toll-Like Receptors in the Immunotherapy Era: Dual-Edged Swords of Tumor Immunity and Clinical Translation.

MedComm (2020). 2025-7-27

[2]
Structural insight into TLR4/MD-2 activation by synthetic LPS mimetics with distinct binding modes.

Nat Commun. 2025-5-5

[3]
Current preclinical models of brain metastasis.

Clin Exp Metastasis. 2024-12-19

[4]
Relationship between GTP binding protein RAB10, toll-like receptor 4, and nuclear factor kappa-B and prognosis in patients with breast cancer.

Sci Rep. 2024-10-7

[5]
The Role of the Toll-like Receptor 2 and the cGAS-STING Pathways in Breast Cancer: Friends or Foes?

Int J Mol Sci. 2023-12-29

[6]
ENO1 Promotes OSCC Migration and Invasion by Orchestrating IL-6 Secretion from Macrophages via a Positive Feedback Loop.

Int J Mol Sci. 2023-1-1

本文引用的文献

[1]
Mapping molecular subtype specific alterations in breast cancer brain metastases identifies clinically relevant vulnerabilities.

Nat Commun. 2022-1-26

[2]
Functional immune cell-astrocyte interactions.

J Exp Med. 2021-9-6

[3]
The PI3K/Akt/mTOR pathway as a preventive target in melanoma brain metastasis.

Neuro Oncol. 2022-2-1

[4]
The CCL2-CCR2 astrocyte-cancer cell axis in tumor extravasation at the brain.

Sci Adv. 2021-6

[5]
Interactions between tumor-derived proteins and Toll-like receptors.

Exp Mol Med. 2020-12

[6]
Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during clinical latency.

Nat Commun. 2020-10-5

[7]
Cellular and Molecular Changes of Brain Metastases-Associated Myeloid Cells during Disease Progression and Therapeutic Response.

iScience. 2020-6-26

[8]
Expression profile of Toll‑like receptors in human breast cancer.

Mol Med Rep. 2019-11-26

[9]
The macro-metastasis/organ parenchyma interface (MMPI) - A hitherto unnoticed area.

Semin Cancer Biol. 2019-10-21

[10]
Tumor-induced peripheral immunosuppression promotes brain metastasis in patients with non-small cell lung cancer.

Cancer Immunol Immunother. 2019-9-5

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索