| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1983279 | The International Journal of Biochemistry & Cell Biology | 2016 | 14 Pages |
Abstract
- Inhibition of (TGF-β)-mediated EMT by vanadium.
- Reduction of mitochondrial ÎÏm in malignant cells triggers EMT blockade.
- Ex vivo down-regulation of CD24/CD44/CD133 CSC markers in cancer patients.
- Synergism between vanadium and carboplatin triggers G0/G1 cell cycle arrest.
- Synergistic mechanism sensitizes tumor cells to carboplatin-induced apoptosis.
Keywords
CSCTGF-βMMPSMACCD24PAI-1MMP-2ROSAIFepithelial mesenchymal transitionTransforming Growth Factor BetaEMTsecond mitochondria-derived activator of caspasescancer stem cellCancer stem cellsmatrix metalloproteinase 2Plasminogen activator inhibitor-1VanadiumMitochondrial membrane potentialReactive oxygen species
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Authors
Savvas Petanidis, Efrosini Kioseoglou, Kalliopi Domvri, Paul Zarogoulidis, Jon M. Carthy, Doxakis Anestakis, Aristidis Moustakas, Athanasios Salifoglou,