Suppr超能文献

上皮-间质转化(EMT)与在纤维状轨道上接触引发的滑动之间存在正定量关系。

Positive Quantitative Relationship between EMT and Contact-Initiated Sliding on Fiber-like Tracks.

作者信息

Milano Daniel F, Natividad Robert J, Saito Yasuhiro, Luo Catherine Y, Muthuswamy Senthil K, Asthagiri Anand R

机构信息

Department of Chemical Engineering, Northeastern University, Boston, Massachusetts.

Department of Bioengineering, Northeastern University, Boston, Massachusetts.

出版信息

Biophys J. 2016 Oct 4;111(7):1569-1574. doi: 10.1016/j.bpj.2016.08.037.

Abstract

Epithelial-mesenchymal transition (EMT) is a complex process by which cells acquire invasive properties that enable escape from the primary tumor. Complete EMT, however, is not required for metastasis: circulating tumor cells exhibit hybrid epithelial-mesenchymal states, and genetic perturbations promoting partial EMT induce metastasis in vivo. An open question is whether and to what extent intermediate stages of EMT promote invasiveness. Here, we investigate this question, building on recent observation of a new invasive property. Migrating cancer cell lines and cells transduced with prometastatic genes slide around other cells on spatially confined, fiberlike micropatterns. We show here that low-dosage/short-duration exposure to transforming growth factor beta (TGFβ) induces partial EMT and enables sliding on narrower (26 μm) micropatterns than untreated counterparts (41 μm). High-dosage/long-duration exposure induces more complete EMT, including disrupted cell-cell contacts and reduced E-cadherin expression, and promotes sliding on the narrowest (15 μm) micropatterns. These results identify a direct and quantitative relationship between EMT and cell sliding and show that EMT-associated invasive sliding is progressive, with cells that undergo partial EMT exhibiting intermediate sliding behavior and cells that transition more completely through EMT displaying maximal sliding. Our findings suggest a model in which fiber maturation and EMT work synergistically to promote invasiveness during cancer progression.

摘要

上皮-间质转化(EMT)是一个复杂的过程,通过该过程细胞获得侵袭特性,从而能够逃离原发性肿瘤。然而,转移并不需要完全的EMT:循环肿瘤细胞表现出混合的上皮-间质状态,促进部分EMT的基因扰动在体内可诱导转移。一个悬而未决的问题是,EMT的中间阶段是否以及在何种程度上促进侵袭性。在此,我们基于最近对一种新的侵袭特性的观察来研究这个问题。迁移的癌细胞系和用促转移基因转导的细胞在空间受限的纤维状微图案上围绕其他细胞滑动。我们在此表明,低剂量/短时间暴露于转化生长因子β(TGFβ)会诱导部分EMT,并使细胞能够在比未处理细胞更窄(26μm)的微图案上滑动(未处理细胞为41μm)。高剂量/长时间暴露会诱导更完全的EMT,包括细胞间接触的破坏和E-钙黏蛋白表达的降低,并促进在最窄(15μm)的微图案上滑动。这些结果确定了EMT与细胞滑动之间的直接定量关系,并表明与EMT相关的侵袭性滑动是渐进的,经历部分EMT的细胞表现出中间滑动行为,而通过EMT更完全转变的细胞表现出最大滑动。我们的研究结果提出了一个模型,即纤维成熟和EMT协同作用以促进癌症进展过程中的侵袭性。

相似文献

1
Positive Quantitative Relationship between EMT and Contact-Initiated Sliding on Fiber-like Tracks.
Biophys J. 2016 Oct 4;111(7):1569-1574. doi: 10.1016/j.bpj.2016.08.037.
2
Regulators of Metastasis Modulate the Migratory Response to Cell Contact under Spatial Confinement.
Biophys J. 2016 Apr 26;110(8):1886-1895. doi: 10.1016/j.bpj.2016.02.040.
4
5
P21 activated kinase-1 mediates transforming growth factor β1-induced prostate cancer cell epithelial to mesenchymal transition.
Biochim Biophys Acta. 2015 May;1853(5):1229-39. doi: 10.1016/j.bbamcr.2015.02.023. Epub 2015 Mar 6.
6
Metformin inhibits the radiation-induced invasive phenotype of esophageal squamous cell carcinoma.
Int J Oncol. 2016 Nov;49(5):1890-1898. doi: 10.3892/ijo.2016.3676. Epub 2016 Aug 31.
8
Py2T murine breast cancer cells, a versatile model of TGFβ-induced EMT in vitro and in vivo.
PLoS One. 2012;7(11):e48651. doi: 10.1371/journal.pone.0048651. Epub 2012 Nov 7.
9
Generation of MCF-7 cells with aggressive metastatic potential in vitro and in vivo.
Breast Cancer Res Treat. 2014 Nov;148(2):269-77. doi: 10.1007/s10549-014-3159-4. Epub 2014 Oct 8.
10
Raf plus TGFbeta-dependent EMT is initiated by endocytosis and lysosomal degradation of E-cadherin.
Oncogene. 2006 Nov 16;25(54):7117-30. doi: 10.1038/sj.onc.1209701. Epub 2006 Jun 5.

引用本文的文献

1
Dynamics of Single-Cell Protein Covariation during Epithelial-Mesenchymal Transition.
J Proteome Res. 2025 Apr 4;24(4):1519-1527. doi: 10.1021/acs.jproteome.4c00277. Epub 2024 Apr 25.
2
Dynamics of single-cell protein covariation during epithelial-mesenchymal transition.
bioRxiv. 2024 Apr 5:2023.12.21.572913. doi: 10.1101/2023.12.21.572913.
3
Picking winners in cell-cell collisions: Wetting, speed, and contact.
Phys Rev E. 2022 Nov;106(5-1):054413. doi: 10.1103/PhysRevE.106.054413.
5
Golgi Stabilization, Not Its Front-Rear Bias, Is Associated with EMT-Enhanced Fibrillar Migration.
Biophys J. 2018 Nov 20;115(10):2067-2077. doi: 10.1016/j.bpj.2018.10.006. Epub 2018 Oct 11.

本文引用的文献

1
Regulators of Metastasis Modulate the Migratory Response to Cell Contact under Spatial Confinement.
Biophys J. 2016 Apr 26;110(8):1886-1895. doi: 10.1016/j.bpj.2016.02.040.
2
Stemness of the hybrid Epithelial/Mesenchymal State in Breast Cancer and Its Association with Poor Survival.
PLoS One. 2015 May 28;10(5):e0126522. doi: 10.1371/journal.pone.0126522. eCollection 2015.
4
Molecular mechanisms of epithelial-mesenchymal transition.
Nat Rev Mol Cell Biol. 2014 Mar;15(3):178-96. doi: 10.1038/nrm3758.
6
MicroRNA-based regulation of epithelial-hybrid-mesenchymal fate determination.
Proc Natl Acad Sci U S A. 2013 Nov 5;110(45):18144-9. doi: 10.1073/pnas.1318192110. Epub 2013 Oct 23.
8
Circulating breast tumor cells exhibit dynamic changes in epithelial and mesenchymal composition.
Science. 2013 Feb 1;339(6119):580-4. doi: 10.1126/science.1228522.
9
Loss of E-cadherin is not a necessity for epithelial to mesenchymal transition in human breast cancer.
Breast Cancer Res Treat. 2013 Feb;138(1):47-57. doi: 10.1007/s10549-013-2415-3. Epub 2013 Jan 22.
10
Rotational motion during three-dimensional morphogenesis of mammary epithelial acini relates to laminin matrix assembly.
Proc Natl Acad Sci U S A. 2013 Jan 2;110(1):163-8. doi: 10.1073/pnas.1201141110. Epub 2012 Dec 17.

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