• 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

胶质母细胞瘤浸润因子 ODZ1 是由微环境信号通过激活 Stat3 依赖性转录途径诱导产生的。

Glioblastoma invasion factor ODZ1 is induced by microenvironmental signals through activation of a Stat3-dependent transcriptional pathway.

机构信息

Genetics Unit, Hospital Universitario Marqués de Valdecilla and Instituto de Investigación Marqués de Valdecilla (IDIVAL), Avda. Valdecilla s/n, 39008, Santander, Spain.

Neurosurgery Service, Hospital Universitario Marqués de Valdecilla and Instituto de Investigación Marqués de Valdecilla (IDIVAL), 39008, Santander, Spain.

出版信息

Sci Rep. 2021 Aug 10;11(1):16196. doi: 10.1038/s41598-021-95753-6.

DOI:10.1038/s41598-021-95753-6
PMID:34376733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8355191/
Abstract

We have previously shown that the transmembrane protein ODZ1 serves for glioblastoma (GBM) cells to invade the surrounding tissue through activation of RhoA/ROCK pathway. However, the transcriptional machinery used by GBM cells to regulate the expression of ODZ1 is unknown. Here we show that interaction with tumor microenvironment elements, mainly activated monocytes through IL-6 secretion, and the extracellular matrix protein fibronectin, induces the Stat3 transcriptional pathway and upregulates ODZ1 which results in GBM cell migration. This signaling route is abrogated by blocking the IL-6 receptor, inhibiting Jak kinases or knocking down Stat3. Furthermore, we have identified a Stat3 responsive element in the ODZ1 gene promoter, about 1 kb from the transcription start site. Luciferase-reporter assays confirmed that the promoter responds to the presence of monocytic cells and this activation is greatly reduced when the Stat3 site is mutated or following treatment with a neutralizing anti-IL-6 receptor antibody or transfecting GBM cells with a dominant negative variant of Stat3. Overall, we show that monocyte-secreted IL-6 and the extracellular matrix protein fibronectin activate the axis Stat3-ODZ1 and promote migration of GBM cells. This is the first described transcriptional mechanism used by tumor cells to promote the expression of the invasion factor ODZ1.

摘要

我们之前已经表明,跨膜蛋白 ODZ1 通过激活 RhoA/ROCK 通路,使神经胶质瘤(GBM)细胞能够侵袭周围组织。然而,GBM 细胞用来调节 ODZ1 表达的转录机制尚不清楚。在这里,我们表明与肿瘤微环境元素的相互作用,主要是通过 IL-6 分泌激活的单核细胞和细胞外基质蛋白纤维连接蛋白,诱导 Stat3 转录途径并上调 ODZ1,从而导致 GBM 细胞迁移。通过阻断 IL-6 受体、抑制 Jak 激酶或敲低 Stat3,可以阻断这种信号通路。此外,我们已经在 ODZ1 基因启动子中鉴定到一个 Stat3 反应元件,距离转录起始位点约 1kb。荧光素酶报告基因检测证实,启动子对单核细胞的存在有反应,而当 Stat3 位点发生突变或用中和抗 IL-6 受体抗体处理或用显性负变异体转染 GBM 细胞时,这种激活大大减少。总的来说,我们表明单核细胞分泌的 IL-6 和细胞外基质蛋白纤维连接蛋白激活了 Stat3-ODZ1 轴,并促进了 GBM 细胞的迁移。这是第一个描述肿瘤细胞用来促进侵袭因子 ODZ1 表达的转录机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/4dfc9c517187/41598_2021_95753_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/bba080f21ab1/41598_2021_95753_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/4ad5dd446058/41598_2021_95753_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/d20328db6fd0/41598_2021_95753_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/734560414591/41598_2021_95753_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/9e36761ecd13/41598_2021_95753_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/7b8fd72d5538/41598_2021_95753_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/4dfc9c517187/41598_2021_95753_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/bba080f21ab1/41598_2021_95753_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/4ad5dd446058/41598_2021_95753_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/d20328db6fd0/41598_2021_95753_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/734560414591/41598_2021_95753_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/9e36761ecd13/41598_2021_95753_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/7b8fd72d5538/41598_2021_95753_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/8355191/4dfc9c517187/41598_2021_95753_Fig7_HTML.jpg

相似文献

1
Glioblastoma invasion factor ODZ1 is induced by microenvironmental signals through activation of a Stat3-dependent transcriptional pathway.胶质母细胞瘤浸润因子 ODZ1 是由微环境信号通过激活 Stat3 依赖性转录途径诱导产生的。
Sci Rep. 2021 Aug 10;11(1):16196. doi: 10.1038/s41598-021-95753-6.
2
ODZ1 allows glioblastoma to sustain invasiveness through a Myc-dependent transcriptional upregulation of RhoA.ODZ1通过Myc依赖的RhoA转录上调使胶质母细胞瘤维持侵袭性。
Oncogene. 2017 Mar 23;36(12):1733-1744. doi: 10.1038/onc.2016.341. Epub 2016 Sep 19.
3
The Invasion Factor ODZ1 Is Upregulated through an Epidermal Growth Factor Receptor-Induced Pathway in Primary Glioblastoma Cells.侵袭因子 ODZ1 通过表皮生长因子受体诱导的途径在原发性脑胶质瘤细胞中上调。
Cells. 2024 Apr 30;13(9):766. doi: 10.3390/cells13090766.
4
HIF2α Upregulates the Migration Factor ODZ1 under Hypoxia in Glioblastoma Stem Cells.低氧诱导因子 2α 在脑胶质瘤干细胞中上调迁移因子 ODZ1。
Int J Mol Sci. 2022 Jan 11;23(2):741. doi: 10.3390/ijms23020741.
5
Hypoxia Can Induce Migration of Glioblastoma Cells Through a Methylation-Dependent Control of Gene Expression.缺氧可通过基因表达的甲基化依赖性调控诱导胶质母细胞瘤细胞迁移。
Front Oncol. 2019 Oct 10;9:1036. doi: 10.3389/fonc.2019.01036. eCollection 2019.
6
TROY signals through JAK1-STAT3 to promote glioblastoma cell migration and resistance.TROY 通过 JAK1-STAT3 信号促进胶质母细胞瘤细胞迁移和耐药性。
Neoplasia. 2020 Sep;22(9):352-364. doi: 10.1016/j.neo.2020.06.005. Epub 2020 Jul 3.
7
NF-κB-induced IL-6 ensures STAT3 activation and tumor aggressiveness in glioblastoma.NF-κB 诱导的 IL-6 确保了胶质母细胞瘤中 STAT3 的激活和肿瘤侵袭性。
PLoS One. 2013 Nov 11;8(11):e78728. doi: 10.1371/journal.pone.0078728. eCollection 2013.
8
RBPJ contributes to the malignancy of glioblastoma and induction of proneural-mesenchymal transition via IL-6-STAT3 pathway.RBPJ 通过 IL-6-STAT3 通路促进胶质母细胞瘤的恶性转化和诱导成神经-间质转化。
Cancer Sci. 2020 Nov;111(11):4166-4176. doi: 10.1111/cas.14642. Epub 2020 Sep 22.
9
Signaling Pathways Regulating the Expression of the Glioblastoma Invasion Factor .调控胶质母细胞瘤侵袭因子表达的信号通路
Biomedicines. 2022 May 10;10(5):1104. doi: 10.3390/biomedicines10051104.
10
Interleukin-6 induces transcriptional activation of vascular endothelial growth factor (VEGF) in astrocytes in vivo and regulates VEGF promoter activity in glioblastoma cells via direct interaction between STAT3 and Sp1.白细胞介素-6在体内诱导星形胶质细胞中血管内皮生长因子(VEGF)的转录激活,并通过信号转导和转录激活因子3(STAT3)与特异性蛋白1(Sp1)之间的直接相互作用调节胶质母细胞瘤细胞中的VEGF启动子活性。
Int J Cancer. 2005 Jun 10;115(2):202-13. doi: 10.1002/ijc.20871.

引用本文的文献

1
The Invasion Factor ODZ1 Is Upregulated through an Epidermal Growth Factor Receptor-Induced Pathway in Primary Glioblastoma Cells.侵袭因子 ODZ1 通过表皮生长因子受体诱导的途径在原发性脑胶质瘤细胞中上调。
Cells. 2024 Apr 30;13(9):766. doi: 10.3390/cells13090766.
2
Profiling the molecular and clinical landscape of glioblastoma utilizing the Oncology Research Information Exchange Network brain cancer database.利用肿瘤学研究信息交流网络脑癌数据库剖析胶质母细胞瘤的分子和临床情况。
Neurooncol Adv. 2024 Mar 27;6(1):vdae046. doi: 10.1093/noajnl/vdae046. eCollection 2024 Jan-Dec.
3
Involvement of Cyclooxygenase-2 in Establishing an Immunosuppressive Microenvironment in Tumorspheres Derived from TMZ-Resistant Glioblastoma Cell Lines and Primary Cultures.

本文引用的文献

1
IL6-receptor antibody tocilizumab as salvage therapy in severe chronic graft-versus-host disease after allogeneic hematopoietic stem cell transplantation: a retrospective analysis.IL6-受体抗体托珠单抗作为异基因造血干细胞移植后严重慢性移植物抗宿主病的挽救治疗:一项回顾性分析。
Ann Hematol. 2020 Apr;99(4):847-853. doi: 10.1007/s00277-020-03968-w. Epub 2020 Feb 21.
2
Hypoxia Can Induce Migration of Glioblastoma Cells Through a Methylation-Dependent Control of Gene Expression.缺氧可通过基因表达的甲基化依赖性调控诱导胶质母细胞瘤细胞迁移。
Front Oncol. 2019 Oct 10;9:1036. doi: 10.3389/fonc.2019.01036. eCollection 2019.
3
环氧化酶-2 参与 TMZ 耐药脑胶质瘤细胞系和原代培养的肿瘤球中免疫抑制微环境的建立。
Cells. 2024 Jan 30;13(3):258. doi: 10.3390/cells13030258.
4
Glioblastoma Microenvironment and Invasiveness: New Insights and Therapeutic Targets.胶质母细胞瘤微环境与侵袭性:新的见解与治疗靶点。
Int J Mol Sci. 2023 Apr 11;24(8):7047. doi: 10.3390/ijms24087047.
5
Signaling Pathways Regulating the Expression of the Glioblastoma Invasion Factor .调控胶质母细胞瘤侵袭因子表达的信号通路
Biomedicines. 2022 May 10;10(5):1104. doi: 10.3390/biomedicines10051104.
6
HIF2α Upregulates the Migration Factor ODZ1 under Hypoxia in Glioblastoma Stem Cells.低氧诱导因子 2α 在脑胶质瘤干细胞中上调迁移因子 ODZ1。
Int J Mol Sci. 2022 Jan 11;23(2):741. doi: 10.3390/ijms23020741.
A STAT3-based gene signature stratifies glioma patients for targeted therapy.
基于 STAT3 的基因特征可对胶质母细胞瘤患者进行靶向治疗分层。
Nat Commun. 2019 Aug 9;10(1):3601. doi: 10.1038/s41467-019-11614-x.
4
Glioblastoma quo vadis: Will migration and invasiveness reemerge as therapeutic targets?胶质母细胞瘤的未来走向:迁移和侵袭性会重新成为治疗靶点吗?
Cancer Treat Rev. 2018 Jul;68:145-154. doi: 10.1016/j.ctrv.2018.06.017. Epub 2018 Jun 26.
5
Chromatin Immunoprecipitation (ChIP) Protocol for Low-abundance Embryonic Samples.低丰度胚胎样本的染色质免疫沉淀(ChIP)实验方案
J Vis Exp. 2017 Aug 29(126):56186. doi: 10.3791/56186.
6
Cellular and Molecular Identity of Tumor-Associated Macrophages in Glioblastoma.胶质母细胞瘤中肿瘤相关巨噬细胞的细胞和分子特征
Cancer Res. 2017 May 1;77(9):2266-2278. doi: 10.1158/0008-5472.CAN-16-2310. Epub 2017 Feb 24.
7
ODZ1 allows glioblastoma to sustain invasiveness through a Myc-dependent transcriptional upregulation of RhoA.ODZ1通过Myc依赖的RhoA转录上调使胶质母细胞瘤维持侵袭性。
Oncogene. 2017 Mar 23;36(12):1733-1744. doi: 10.1038/onc.2016.341. Epub 2016 Sep 19.
8
Human glioblastoma-associated microglia/monocytes express a distinct RNA profile compared to human control and murine samples.与人类对照样本和小鼠样本相比,人类胶质母细胞瘤相关的小胶质细胞/单核细胞表达独特的RNA谱。
Glia. 2016 Aug;64(8):1416-36. doi: 10.1002/glia.23014.
9
Role of interleukin-6 in cancer progression and therapeutic resistance.白细胞介素-6在癌症进展和治疗耐药中的作用。
Tumour Biol. 2016 Sep;37(9):11553-11572. doi: 10.1007/s13277-016-5098-7. Epub 2016 Jun 3.
10
STAT3 activation in response to IL-6 is prolonged by the binding of IL-6 receptor to EGF receptor.STAT3 的激活是对白细胞介素-6(IL-6)反应的一种表现,这种激活可通过白细胞介素-6 受体(IL-6R)与表皮生长因子受体(EGF receptor)的结合而延长。
Proc Natl Acad Sci U S A. 2013 Oct 15;110(42):16975-80. doi: 10.1073/pnas.1315862110. Epub 2013 Sep 30.