Stretch Induces Invasive Phenotypes in Breast Cells Due to Activation of Aerobic-Glycolysis-Related Pathways.
breast cancer
cancer invasion
glycolysis
mechanical stretch
Journal
Advanced biosystems
ISSN: 2366-7478
Titre abrégé: Adv Biosyst
Pays: Germany
ID NLM: 101711718
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
received:
28
10
2018
revised:
22
03
2019
entrez:
11
7
2020
pubmed:
11
7
2020
medline:
25
9
2020
Statut:
ppublish
Résumé
It is increasingly being accepted that cells' physiological functions are substantially dependent on the mechanical characteristics of their surrounding tissue. This is mainly due to the key role of biomechanical forces on cells and their nucleus' shapes, which have the capacity to regulate chromatin conformation and thus gene regulations. Therefore, it is reasonable to postulate that altering the biomechanical properties of tissue may have the capacity to change cell functions. Here, the role of cell stretching (as a model of biomechanical variations) is probed in cell migration and invasion capacity using human normal and cancerous breast cells. By several analyses (i.e., scratch assay, invasion to endothelial barrier, real-time RNA sequencing, confocal imaging, patch clamp, etc.), it is revealed that the cell-stretching process could increase the migration and invasion capabilities of normal and cancerous cells, respectively. More specifically, it is found that poststretched breast cancer cells are found in low grades of invasion; they substantially upregulate the expression of manganese-dependent superoxide dismutase (MnSOD) through activation of H-Ras proteins, which subsequently induce aerobic glycolysis followed by an overproduction of matrix metalloproteinases (MMP)-reinforced filopodias. Presence of such invadopodias facilitates targeting of the endothelial layer, and increased invasive behaviors in breast cells are observed.
Identifiants
pubmed: 32648669
doi: 10.1002/adbi.201800294
doi:
Substances chimiques
Neoplasm Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1800294Informations de copyright
© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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