Fluidity of Poly (ε-Caprolactone)-Based Material Induces Epithelial-to-Mesenchymal Transition.
Antigens, CD
/ metabolism
Biocompatible Materials
Cadherins
/ metabolism
Cell Adhesion
Cell Line, Tumor
Cell Proliferation
Epithelial-Mesenchymal Transition
/ drug effects
Humans
MCF-7 Cells
Mesenchymal Stem Cells
/ metabolism
Microscopy, Confocal
Molecular Weight
Polyesters
/ metabolism
Pressure
Signal Transduction
Transforming Growth Factor beta
/ metabolism
Vimentin
/ metabolism
dynamic material
epithelial to mesenchymal transition
fluidity
mechanotransduction
poly (ε-caprolactone)
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
04 Mar 2020
04 Mar 2020
Historique:
received:
28
01
2020
revised:
26
02
2020
accepted:
27
02
2020
entrez:
8
3
2020
pubmed:
8
3
2020
medline:
5
1
2021
Statut:
epublish
Résumé
We propose the potential studies on material fluidity to induce epithelial to mesenchymal transition (EMT) in MCF-7 cells. In this study, we examined for the first time the effect of material fluidity on EMT using poly(ε-caprolactone- The fluidity was altered by chemically crosslinking the polymer networks. The crosslinked P(CL- We observed that MCF-7 cells on low fluidic substrates decreased the expression of E-cadherin, an epithelial marker, and increased expression of vimentin, a mesenchymal marker. This showed that the cells lose their epithelial phenotype and gain a mesenchymal property. On the other hand, MCF-7 cells on high fluidic substrates maintained their epithelial phenotype, suggesting that the cells did not undergo EMT. Considering these results as the fundamental information for material fluidity induced EMT, our system could be used to regulate the degree of EMT by turning the fluidity of the material.
Sections du résumé
BACKGROUND
BACKGROUND
We propose the potential studies on material fluidity to induce epithelial to mesenchymal transition (EMT) in MCF-7 cells. In this study, we examined for the first time the effect of material fluidity on EMT using poly(ε-caprolactone-
METHODS
METHODS
The fluidity was altered by chemically crosslinking the polymer networks. The crosslinked P(CL-
RESULTS
RESULTS
We observed that MCF-7 cells on low fluidic substrates decreased the expression of E-cadherin, an epithelial marker, and increased expression of vimentin, a mesenchymal marker. This showed that the cells lose their epithelial phenotype and gain a mesenchymal property. On the other hand, MCF-7 cells on high fluidic substrates maintained their epithelial phenotype, suggesting that the cells did not undergo EMT.
CONCLUSION
CONCLUSIONS
Considering these results as the fundamental information for material fluidity induced EMT, our system could be used to regulate the degree of EMT by turning the fluidity of the material.
Identifiants
pubmed: 32143443
pii: ijms21051757
doi: 10.3390/ijms21051757
pmc: PMC7084864
pii:
doi:
Substances chimiques
Antigens, CD
0
Biocompatible Materials
0
CDH1 protein, human
0
Cadherins
0
Polyesters
0
Transforming Growth Factor beta
0
VIM protein, human
0
Vimentin
0
polycaprolactone
24980-41-4
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Japan Society for the Promotion of Science
ID : 19H04476
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