• 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

自噬对上皮-间质转化的调控:胶质母细胞瘤生物学的新视角

EMT Regulation by Autophagy: A New Perspective in Glioblastoma Biology.

作者信息

Colella Barbara, Faienza Fiorella, Di Bartolomeo Sabrina

机构信息

Department of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy.

Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy.

出版信息

Cancers (Basel). 2019 Mar 6;11(3):312. doi: 10.3390/cancers11030312.

DOI:10.3390/cancers11030312
PMID:30845654
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6468412/
Abstract

Epithelial-to-mesenchymal transition (EMT) and its reverse process MET naturally occur during development and in tissue repair in vertebrates. EMT is also recognized as the crucial event by which cancer cells acquire an invasive phenotype through the activation of specific transcription factors and signalling pathways. Even though glial cells have a mesenchymal phenotype, an EMT-like process tends to exacerbate it during gliomagenesis and progression to more aggressive stages of the disease. Autophagy is an evolutionary conserved degradative process that cells use in order to maintain a proper homeostasis, and defects in autophagy have been associated to several pathologies including cancer. Besides modulating cell resistance or sensitivity to therapy, autophagy also affects the migration and invasion capabilities of tumor cells. Despite this evidence, few papers are present in literature about the involvement of autophagy in EMT-like processes in glioblastoma (GBM) so far. This review summarizes the current understanding of the interplay between autophagy and EMT in cancer, with special regard to GBM model. As the invasive behaviour is a hallmark of GBM aggressiveness, defining a new link between autophagy and EMT can open a novel scenario for targeting these processes in future therapeutical approaches.

摘要

上皮-间质转化(EMT)及其逆向过程间充质-上皮转化(MET)在脊椎动物的发育和组织修复过程中自然发生。EMT也被认为是癌细胞通过激活特定转录因子和信号通路获得侵袭性表型的关键事件。尽管胶质细胞具有间充质表型,但在胶质瘤发生过程中,类似EMT的过程往往会使其加剧,并促使疾病发展到更具侵袭性的阶段。自噬是一种进化保守的降解过程,细胞利用它来维持适当的内环境稳定,自噬缺陷与包括癌症在内的多种疾病有关。除了调节细胞对治疗的抗性或敏感性外,自噬还影响肿瘤细胞的迁移和侵袭能力。尽管有这些证据,但迄今为止,关于自噬在胶质母细胞瘤(GBM)类似EMT过程中的作用,文献中报道较少。本综述总结了目前对癌症中自噬与EMT相互作用的理解,特别是关于GBM模型。由于侵袭行为是GBM侵袭性的标志,确定自噬与EMT之间的新联系可为未来治疗方法中针对这些过程开辟新的前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff4a/6468412/13491a9e714f/cancers-11-00312-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff4a/6468412/90d351f1e77b/cancers-11-00312-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff4a/6468412/13491a9e714f/cancers-11-00312-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff4a/6468412/90d351f1e77b/cancers-11-00312-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff4a/6468412/13491a9e714f/cancers-11-00312-g002.jpg

相似文献

1
EMT Regulation by Autophagy: A New Perspective in Glioblastoma Biology.自噬对上皮-间质转化的调控:胶质母细胞瘤生物学的新视角
Cancers (Basel). 2019 Mar 6;11(3):312. doi: 10.3390/cancers11030312.
2
Autophagy induction impairs Wnt/β-catenin signalling through β-catenin relocalisation in glioblastoma cells.自噬诱导通过β-连环蛋白在神经胶质瘤细胞中的重新定位来损害 Wnt/β-连环蛋白信号通路。
Cell Signal. 2019 Jan;53:357-364. doi: 10.1016/j.cellsig.2018.10.017. Epub 2018 Oct 26.
3
Multifaceted WNT Signaling at the Crossroads Between Epithelial-Mesenchymal Transition and Autophagy in Glioblastoma.胶质母细胞瘤中上皮-间质转化与自噬交叉点上的多面WNT信号传导
Front Oncol. 2020 Nov 12;10:597743. doi: 10.3389/fonc.2020.597743. eCollection 2020.
4
Autophagy induction impairs migration and invasion by reversing EMT in glioblastoma cells.自噬诱导通过逆转胶质母细胞瘤细胞中的上皮-间质转化来损害迁移和侵袭能力。
Mol Oncol. 2015 Oct;9(8):1612-25. doi: 10.1016/j.molonc.2015.04.016. Epub 2015 May 13.
5
MIR517C inhibits autophagy and the epithelial-to-mesenchymal (-like) transition phenotype in human glioblastoma through KPNA2-dependent disruption of TP53 nuclear translocation.MIR517C通过依赖KPNA2破坏TP53核转位来抑制人胶质母细胞瘤中的自噬及上皮-间质(样)转化表型。
Autophagy. 2015;11(12):2213-32. doi: 10.1080/15548627.2015.1108507.
6
miR-504 suppresses mesenchymal phenotype of glioblastoma by directly targeting the FZD7-mediated Wnt-β-catenin pathway.miR-504 通过直接靶向 FZD7 介导的 Wnt-β-catenin 通路抑制胶质母细胞瘤的间充质表型。
J Exp Clin Cancer Res. 2019 Aug 16;38(1):358. doi: 10.1186/s13046-019-1370-1.
7
A New Investigational Perspective for Purines Against Glioblastoma Invasiveness.嘌呤类药物抗脑胶质瘤侵袭的新研究视角。
Curr Drug Targets. 2018;19(16):1871-1881. doi: 10.2174/1389450119666180226123819.
8
The Epithelial-to-Mesenchymal Transition-Like Process in Glioblastoma: An Updated Systematic Review and In Silico Investigation.胶质母细胞瘤中的上皮间质转化样过程:一项更新的系统评价和计算机模拟研究。
Med Res Rev. 2017 Mar;37(2):271-313. doi: 10.1002/med.21408. Epub 2016 Sep 12.
9
Verbascoside suppresses the migration and invasion of human glioblastoma cells via targeting c-Met-mediated epithelial-mesenchymal transition.毛蕊花糖苷通过靶向 c-Met 介导的上皮-间充质转化抑制人脑胶质瘤细胞的迁移和侵袭。
Biochem Biophys Res Commun. 2019 Jul 5;514(4):1270-1277. doi: 10.1016/j.bbrc.2019.05.096. Epub 2019 May 18.
10
Interplay between microRNAs and WNT/β-catenin signalling pathway regulates epithelial-mesenchymal transition in cancer.微小RNA与WNT/β-连环蛋白信号通路之间的相互作用调节癌症中的上皮-间质转化。
Eur J Cancer. 2015 Aug;51(12):1638-49. doi: 10.1016/j.ejca.2015.04.021. Epub 2015 May 26.

引用本文的文献

1
Shikonin inhibits epithelial-mesenchymal transition in glioblastoma cells by upregulating p53 and promoting miR-361-5p level to suppress ZEB1 expression.紫草素通过上调p53和提高miR-361-5p水平以抑制锌指蛋白E盒结合因子1(ZEB1)的表达,从而抑制胶质母细胞瘤细胞的上皮-间质转化。
BMC Neurosci. 2025 Jul 1;26(1):37. doi: 10.1186/s12868-025-00956-6.
2
PDGF-D Promotes Epithelial-Mesenchymal Transition of Glioma Cells Through the NF-κB/NOTCH1 Pathway.血小板源性生长因子-D通过NF-κB/Notch1信号通路促进胶质瘤细胞上皮-间质转化
Cancer Med. 2025 Jun;14(12):e71002. doi: 10.1002/cam4.71002.
3
Autophagy as a potential therapeutic target in regulating improper cellular proliferation.

本文引用的文献

1
Autophagy induction impairs Wnt/β-catenin signalling through β-catenin relocalisation in glioblastoma cells.自噬诱导通过β-连环蛋白在神经胶质瘤细胞中的重新定位来损害 Wnt/β-连环蛋白信号通路。
Cell Signal. 2019 Jan;53:357-364. doi: 10.1016/j.cellsig.2018.10.017. Epub 2018 Oct 26.
2
EGFR-Signaling and Autophagy: How they Fit in the Cancer Landscape.表皮生长因子受体信号传导与自噬:它们在癌症格局中的作用机制
J Adenocarcinoma. 2016;1(2).
3
Starvation-induced autophagy promotes the invasion and migration of human bladder cancer cells via TGF-β1/Smad3-mediated epithelial-mesenchymal transition activation.
自噬作为调节细胞异常增殖的潜在治疗靶点。
Front Pharmacol. 2025 May 15;16:1579183. doi: 10.3389/fphar.2025.1579183. eCollection 2025.
4
TMBIM1 promotes epithelial mesenchymal transition by accelerating autophagic degradation of E-cadherin in glioblastoma.TMBIM1通过加速胶质母细胞瘤中E-钙黏蛋白的自噬降解来促进上皮-间质转化。
Sci Rep. 2025 May 20;15(1):17488. doi: 10.1038/s41598-025-01699-4.
5
Proteomic Profiling of Pre- and Post-Surgery Saliva of Glioblastoma Patients: A Pilot Investigation.胶质母细胞瘤患者手术前后唾液的蛋白质组学分析:一项初步研究。
Int J Mol Sci. 2024 Dec 3;25(23):12984. doi: 10.3390/ijms252312984.
6
Epigenetic dysregulation in glioblastoma: potential pathways to precision medicine.胶质母细胞瘤中的表观遗传失调:精准医学的潜在途径。
Neurogenetics. 2024 Nov 25;26(1):5. doi: 10.1007/s10048-024-00793-5.
7
The Role of Curcumin in Cancer: A Focus on the PI3K/Akt Pathway.姜黄素在癌症中的作用:聚焦于PI3K/Akt信号通路。
Cancers (Basel). 2024 Apr 18;16(8):1554. doi: 10.3390/cancers16081554.
8
Let-7a-3p overexpression increases chemosensitivity to carmustine and synergistically promotes autophagy and suppresses cell survival in U87MG glioblastoma cancer cells.Let-7a-3p 过表达增加卡莫司汀化疗敏感性,并协同促进自噬和抑制 U87MG 脑胶质瘤癌细胞存活。
Naunyn Schmiedebergs Arch Pharmacol. 2024 Sep;397(9):6903-6918. doi: 10.1007/s00210-024-03060-4. Epub 2024 Apr 8.
9
Identification and validation of autophagy-related genes in SSc.系统性硬化症中自噬相关基因的鉴定与验证
Open Med (Wars). 2024 Apr 5;19(1):20240942. doi: 10.1515/med-2024-0942. eCollection 2024.
10
GPR65 sensing tumor-derived lactate induces HMGB1 release from TAM via the cAMP/PKA/CREB pathway to promote glioma progression.GPR65 感应肿瘤来源的乳酸通过 cAMP/PKA/CREB 通路诱导 TAM 释放 HMGB1,从而促进胶质瘤的进展。
J Exp Clin Cancer Res. 2024 Apr 4;43(1):105. doi: 10.1186/s13046-024-03025-8.
饥饿诱导的自噬通过 TGF-β1/Smad3 介导的上皮-间充质转化激活促进人膀胱癌细胞的侵袭和迁移。
J Cell Biochem. 2019 Apr;120(4):5118-5127. doi: 10.1002/jcb.27788. Epub 2018 Oct 15.
4
Autophagy induces transforming growth factor-β-dependent epithelial-mesenchymal transition in hepatocarcinoma cells through cAMP response element binding signalling.自噬通过 cAMP 反应元件结合信号诱导肝癌细胞中的转化生长因子-β 依赖性上皮-间充质转化。
J Cell Mol Med. 2018 Nov;22(11):5518-5532. doi: 10.1111/jcmm.13825. Epub 2018 Aug 22.
5
Maternal exposure to di-n-butyl phthalate (DBP) promotes epithelial-mesenchymal transition via regulation of autophagy in uroepithelial cell.母体暴露于邻苯二甲酸二丁酯(DBP)通过调节尿路上皮细胞自噬促进上皮-间充质转化。
Toxicology. 2018 Aug 1;406-407:114-122. doi: 10.1016/j.tox.2018.07.013. Epub 2018 Jul 24.
6
DRAM1 regulates the migration and invasion of hepatoblastoma cells via autophagy-EMT pathway.DRAM1通过自噬-上皮-间质转化途径调节肝母细胞瘤细胞的迁移和侵袭。
Oncol Lett. 2018 Aug;16(2):2427-2433. doi: 10.3892/ol.2018.8937. Epub 2018 Jun 8.
7
Chloroquine inhibits autophagic flux by decreasing autophagosome-lysosome fusion.氯喹通过减少自噬体-溶酶体融合来抑制自噬流。
Autophagy. 2018;14(8):1435-1455. doi: 10.1080/15548627.2018.1474314. Epub 2018 Jul 20.
8
Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis.自噬有助于子宫内膜异位症中子宫内膜上皮细胞缺氧诱导的上皮间质转化。
Biol Reprod. 2018 Nov 1;99(5):968-981. doi: 10.1093/biolre/ioy128.
9
Knockdown of Beclin-1 impairs epithelial-mesenchymal transition of colon cancer cells.敲低Beclin-1会损害结肠癌细胞的上皮-间质转化。
J Cell Biochem. 2018 Aug;119(8):7022-7031. doi: 10.1002/jcb.26912. Epub 2018 May 8.
10
PP242 Counteracts Glioblastoma Cell Proliferation, Migration, Invasiveness and Stemness Properties by Inhibiting mTORC2/AKT.PP242通过抑制mTORC2/AKT来对抗胶质母细胞瘤细胞的增殖、迁移、侵袭和干性特性。
Front Cell Neurosci. 2018 Apr 10;12:99. doi: 10.3389/fncel.2018.00099. eCollection 2018.