• 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

肿瘤细胞去分化:肿瘤转移和复发的可塑性驱动策略。

Cancer Cell De-Differentiation: Plasticity-Driven Stratagem For Tumor Metastasis and Recurrence.

机构信息

INSERM U976, Université Paris Cité, Paris, France.

出版信息

Curr Stem Cell Res Ther. 2023;18(1):54-61. doi: 10.2174/1574888X17666220608101852.

DOI:10.2174/1574888X17666220608101852
PMID:35676837
Abstract

Tumor recurrence is a colossal challenge in clinical oncology. This multifactorial problem is attributed to the emergence of additional genetic mutations and the presence of dormant cancer cells. However, the plasticity of non-stem cancer cells and the acquisition of cancer stem cell (CSC) functionality is another contributing factor to tumor recurrence. Herein, I focus attention on the mechanisms that fuel cancer cell de-differentiation and the interplay between intra-cellular regulators and tumor microenvironment (TME) landscape that promotes cancer cell stemness. Our understanding of the mechanisms underlying tumor cell de-differentiation is crucial for developing innovative therapeutic strategies that prevent cancer from ever recurring.

摘要

肿瘤复发是临床肿瘤学面临的巨大挑战。这个多因素问题归因于额外基因突变的出现和休眠癌细胞的存在。然而,非干细胞癌细胞的可塑性和获得癌症干细胞(CSC)功能也是肿瘤复发的另一个因素。在此,我重点关注促进癌细胞去分化的机制以及细胞内调节剂和肿瘤微环境(TME)景观之间的相互作用,这些相互作用促进了癌细胞的干性。我们对肿瘤细胞去分化背后机制的理解对于开发创新性治疗策略以防止癌症复发至关重要。

相似文献

1
Cancer Cell De-Differentiation: Plasticity-Driven Stratagem For Tumor Metastasis and Recurrence.肿瘤细胞去分化:肿瘤转移和复发的可塑性驱动策略。
Curr Stem Cell Res Ther. 2023;18(1):54-61. doi: 10.2174/1574888X17666220608101852.
2
Cancer stem cell (a)symmetry & plasticity: Tumorigenesis and therapy relevance.癌症干细胞(a)对称性与可塑性:肿瘤发生与治疗相关性。
Life Sci. 2019 Aug 15;231:116520. doi: 10.1016/j.lfs.2019.05.076. Epub 2019 May 31.
3
Dormant tumor cells expressing LOXL2 acquire a stem-like phenotype mediating their transition to proliferative growth.表达赖氨酰氧化酶样蛋白2(LOXL2)的休眠肿瘤细胞获得一种干细胞样表型,介导其向增殖性生长的转变。
Oncotarget. 2016 Nov 1;7(44):71362-71377. doi: 10.18632/oncotarget.12109.
4
Tumor dormancy as an alternative step in the development of chemoresistance and metastasis - clinical implications.肿瘤休眠作为化疗耐药性和转移发展的替代步骤——临床意义。
Cell Oncol (Dordr). 2020 Apr;43(2):155-176. doi: 10.1007/s13402-019-00467-7. Epub 2019 Aug 7.
5
The Role of the Microenvironment and Immune System in Regulating Stem Cell Fate in Cancer.微环境和免疫系统在调节癌症干细胞命运中的作用。
Trends Cancer. 2021 Jul;7(7):624-634. doi: 10.1016/j.trecan.2020.12.014. Epub 2021 Jan 26.
6
Tuning Cancer Fate: Tumor Microenvironment's Role in Cancer Stem Cell Quiescence and Reawakening.调控癌症命运:肿瘤微环境在癌症干细胞静止和再激活中的作用。
Front Immunol. 2020 Oct 21;11:2166. doi: 10.3389/fimmu.2020.02166. eCollection 2020.
7
Tumor dormancy and cancer stem cells: two sides of the same coin?肿瘤休眠与癌症干细胞:同一枚硬币的两面?
Adv Exp Med Biol. 2013;734:145-79. doi: 10.1007/978-1-4614-1445-2_8.
8
The opposing effects of interferon-beta and oncostatin-M as regulators of cancer stem cell plasticity in triple-negative breast cancer.干扰素-β和肿瘤坏死因子-α作为三阴性乳腺癌中癌症干细胞可塑性的调节剂的拮抗作用。
Breast Cancer Res. 2019 Apr 29;21(1):54. doi: 10.1186/s13058-019-1136-x.
9
Cellular Plasticity-Targeted Therapy in Head and Neck Cancers.头颈部癌症中的细胞可塑性靶向治疗。
J Dent Res. 2018 Jun;97(6):654-664. doi: 10.1177/0022034518756351. Epub 2018 Feb 27.
10
Cancer stem cells and the tumor microenvironment: interplay in tumor heterogeneity.癌症干细胞与肿瘤微环境:肿瘤异质性中的相互作用
Connect Tissue Res. 2015;56(5):414-25. doi: 10.3109/03008207.2015.1066780. Epub 2015 Aug 20.

引用本文的文献

1
Deciphering the Role of Cancer Stem Cells: Drivers of Tumor Evolution, Therapeutic Resistance, and Precision Medicine Strategies.解读癌症干细胞的作用:肿瘤进化、治疗抗性及精准医学策略的驱动因素
Cancers (Basel). 2025 Jan 24;17(3):382. doi: 10.3390/cancers17030382.

本文引用的文献

1
The Gene Signature of Activated M-CSF-Primed Human Monocyte-Derived Macrophages Is IL-10-Dependent.激活的 M-CSF 诱导的人单核细胞来源的巨噬细胞的基因特征依赖于 IL-10。
J Innate Immun. 2022;14(3):243-256. doi: 10.1159/000519305. Epub 2021 Oct 20.
2
Tumor microenvironment-based screening repurposes drugs targeting cancer stem cells and cancer-associated fibroblasts.基于肿瘤微环境的筛选使针对癌症干细胞和癌症相关成纤维细胞的药物得到重新利用。
Theranostics. 2021 Sep 21;11(19):9667-9686. doi: 10.7150/thno.62676. eCollection 2021.
3
Spatially confined sub-tumor microenvironments in pancreatic cancer.
胰腺癌中空间受限的肿瘤微环境。
Cell. 2021 Oct 28;184(22):5577-5592.e18. doi: 10.1016/j.cell.2021.09.022. Epub 2021 Oct 12.
4
The roles of tumor-derived exosomes in altered differentiation, maturation and function of dendritic cells.肿瘤来源的外泌体在树突状细胞分化、成熟和功能改变中的作用。
Mol Cancer. 2021 Jun 2;20(1):83. doi: 10.1186/s12943-021-01376-w.
5
Tumor Dormancy: Implications for Invasion and Metastasis.肿瘤休眠:对侵袭和转移的影响。
Int J Mol Sci. 2021 May 4;22(9):4862. doi: 10.3390/ijms22094862.
6
The Post-Translational Regulation of Epithelial-Mesenchymal Transition-Inducing Transcription Factors in Cancer Metastasis.癌症转移中上皮-间质转化诱导转录因子的翻译后调控
Int J Mol Sci. 2021 Mar 30;22(7):3591. doi: 10.3390/ijms22073591.
7
Cancer recurrence and lethality are enabled by enhanced survival and reversible cell cycle arrest of polyaneuploid cells.癌症的复发和致死率是由多倍体细胞的生存能力增强和可逆的细胞周期停滞所导致的。
Proc Natl Acad Sci U S A. 2021 Feb 16;118(7). doi: 10.1073/pnas.2020838118.
8
ABL001, a Bispecific Antibody Targeting VEGF and DLL4, with Chemotherapy, Synergistically Inhibits Tumor Progression in Xenograft Models.ABL001,一种同时靶向 VEGF 和 DLL4 的双特异性抗体,与化疗联合使用,在异种移植模型中协同抑制肿瘤进展。
Int J Mol Sci. 2020 Dec 29;22(1):241. doi: 10.3390/ijms22010241.
9
Metabolic Regulation of Epigenetic Modifications and Cell Differentiation in Cancer.癌症中表观遗传修饰和细胞分化的代谢调控
Cancers (Basel). 2020 Dec 16;12(12):3788. doi: 10.3390/cancers12123788.
10
Roles of the HGF/Met signaling in head and neck squamous cell carcinoma: Focus on tumor immunity (Review).HGF/Met 信号在头颈部鳞状细胞癌中的作用:聚焦于肿瘤免疫(综述)。
Oncol Rep. 2020 Dec;44(6):2337-2344. doi: 10.3892/or.2020.7799. Epub 2020 Oct 9.