Suppr超能文献

上皮-间质可塑性与癌症干细胞之间的通讯:对癌症进展的新见解

Communication Between Epithelial-Mesenchymal Plasticity and Cancer Stem Cells: New Insights Into Cancer Progression.

作者信息

Zheng Xiaobo, Dai Fuzhen, Feng Lei, Zou Hong, Feng Li, Xu Mingqing

机构信息

Department of Liver Surgery, West China Hospital, Sichuan University, Chengdu, China.

Department of General Surgery, The First People's Hospital of Longquanyi District, Chengdu, China.

出版信息

Front Oncol. 2021 Apr 21;11:617597. doi: 10.3389/fonc.2021.617597. eCollection 2021.

Abstract

The epithelial-mesenchymal transition (EMT) is closely associated with the acquisition of aggressive traits by carcinoma cells and is considered responsible for metastasis, relapse, and chemoresistance. Molecular links between the EMT and cancer stem cells (CSCs) have indicated that EMT processes play important roles in the expression of CSC-like properties. It is generally thought that EMT-related transcription factors (EMT-TFs) need to be downregulated to confer an epithelial phenotype to mesenchymal cells and increase cell proliferation, thereby promoting metastasis formation. However, the genetic and epigenetic mechanisms that regulate EMT and CSC activation are contradictory. Emerging evidence suggests that EMT need not be a binary model and instead a hybrid epithelial/mesenchymal state. This dynamic process correlates with epithelial-mesenchymal plasticity, which indicates a contradictory role of EMT during cancer progression. Recent studies have linked the epithelial-mesenchymal plasticity and stem cell-like traits, providing new insights into the conflicting relationship between EMT and CSCs. In this review, we examine the current knowledge about the interplay between epithelial-mesenchymal plasticity and CSCs in cancer biology and evaluate the controversies and future perspectives. Understanding the biology of epithelial-mesenchymal plasticity and CSCs and their implications in therapeutic treatment may provide new opportunities for targeted intervention.

摘要

上皮-间质转化(EMT)与癌细胞侵袭性特征的获得密切相关,被认为是转移、复发和化疗耐药的原因。EMT与癌症干细胞(CSCs)之间的分子联系表明,EMT过程在CSC样特性的表达中起重要作用。一般认为,需要下调EMT相关转录因子(EMT-TFs),以使间充质细胞获得上皮表型并增加细胞增殖,从而促进转移灶形成。然而,调节EMT和CSC激活的遗传和表观遗传机制相互矛盾。新出现的证据表明,EMT不一定是二元模型,而是一种混合的上皮/间充质状态。这一动态过程与上皮-间质可塑性相关,这表明EMT在癌症进展过程中具有矛盾的作用。最近的研究将上皮-间质可塑性与干细胞样特征联系起来,为EMT和CSCs之间的矛盾关系提供了新的见解。在这篇综述中,我们研究了癌症生物学中关于上皮-间质可塑性与CSCs之间相互作用的现有知识,并评估了相关争议和未来展望。了解上皮-间质可塑性和CSCs的生物学特性及其在治疗中的意义,可能为靶向干预提供新的机会。

相似文献

1
Communication Between Epithelial-Mesenchymal Plasticity and Cancer Stem Cells: New Insights Into Cancer Progression.
Front Oncol. 2021 Apr 21;11:617597. doi: 10.3389/fonc.2021.617597. eCollection 2021.
6
Cancer stem cells and epithelial-mesenchymal transition: concepts and molecular links.
Semin Cancer Biol. 2012 Oct;22(5-6):396-403. doi: 10.1016/j.semcancer.2012.04.001. Epub 2012 Apr 23.
7
EMT imparts cancer stemness and plasticity: new perspectives and therapeutic potential.
Front Biosci (Landmark Ed). 2021 Jan 1;26(2):238-265. doi: 10.2741/4893.
8
Exploiting transcription factors to target EMT and cancer stem cells for tumor modulation and therapy.
Semin Cancer Biol. 2024 May;100:1-16. doi: 10.1016/j.semcancer.2024.03.002. Epub 2024 Mar 19.

引用本文的文献

1
Analyzing the Blueprint: Exploring the Molecular Profile of Metastasis and Therapeutic Resistance.
Int J Mol Sci. 2025 Jul 20;26(14):6954. doi: 10.3390/ijms26146954.
3
The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.
J Biol Chem. 2024 Dec;300(12):107994. doi: 10.1016/j.jbc.2024.107994. Epub 2024 Nov 14.
5
Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, , and through NFκB-signaling.
Oncoimmunology. 2024 Aug 21;13(1):2393442. doi: 10.1080/2162402X.2024.2393442. eCollection 2024.
6
MEX3A promotes colorectal cancer migration, invasion and EMT via regulating the Wnt/β-catenin signaling pathway.
J Cancer Res Clin Oncol. 2024 Jun 25;150(6):319. doi: 10.1007/s00432-024-05845-9.
7
Glycogen synthase kinase 3β: the nexus of chemoresistance, invasive capacity, and cancer stemness in pancreatic cancer.
Cancer Drug Resist. 2024 Jan 31;7:4. doi: 10.20517/cdr.2023.84. eCollection 2024.
9
Role of Vitamin C in Targeting Cancer Stem Cells and Cellular Plasticity.
Cancers (Basel). 2023 Nov 30;15(23):5657. doi: 10.3390/cancers15235657.
10
Epithelial-mesenchymal transition in cancer stem cells: Therapeutic implications.
J Oral Maxillofac Pathol. 2023 Apr-Jun;27(2):359-363. doi: 10.4103/jomfp.jomfp_308_22. Epub 2023 Jul 13.

本文引用的文献

2
Inhibition of the Wnt Signalling Pathway: An Avenue to Control Breast Cancer Aggressiveness.
Int J Mol Sci. 2020 Nov 28;21(23):9069. doi: 10.3390/ijms21239069.
4
EMT, cancer stem cells and autophagy; The three main axes of metastasis.
Biomed Pharmacother. 2021 Jan;133:110909. doi: 10.1016/j.biopha.2020.110909. Epub 2020 Nov 20.
5
Emerging Concepts of Hybrid Epithelial-to-Mesenchymal Transition in Cancer Progression.
Biomolecules. 2020 Nov 16;10(11):1561. doi: 10.3390/biom10111561.
6
Metastasis: crosstalk between tissue mechanics and tumour cell plasticity.
Br J Cancer. 2021 Jan;124(1):49-57. doi: 10.1038/s41416-020-01150-7. Epub 2020 Nov 18.
7
Exosomes and breast cancer drug resistance.
Cell Death Dis. 2020 Nov 17;11(11):987. doi: 10.1038/s41419-020-03189-z.
8
Cortactin in Epithelial-Mesenchymal Transition.
Front Cell Dev Biol. 2020 Oct 20;8:585619. doi: 10.3389/fcell.2020.585619. eCollection 2020.
9
Epigenetic targeting of neuropilin-1 prevents bypass signaling in drug-resistant breast cancer.
Oncogene. 2021 Jan;40(2):322-333. doi: 10.1038/s41388-020-01530-6. Epub 2020 Oct 30.
10
Co-Expression of Stem Cell and Epithelial Mesenchymal Transition Markers in Circulating Tumor Cells of Bladder Cancer Patients.
Onco Targets Ther. 2020 Oct 22;13:10739-10748. doi: 10.2147/OTT.S259240. eCollection 2020.

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

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验