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Nanoparticle mediated alteration of EMT dynamics: an approach to modulate cancer therapeutics

Sen, Plaboni, Saha, Muktashree, Ghosh, Siddhartha Sankar·2020·Materials Advances
DOI 10.1039/d0ma00455c
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Abstract

Metastasis is the cause of approximately 90% of cancer-related morbidities and mortalities, which is ascribed to the phenomenon of EMT (epithelial to mesenchymal transition). The nanoparticle mediated suppression of EMT exhibit strong therapeutic modalities.

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Fig. 2 The pathways facilitating EMT. The pathways known to induce EMT by activating the downstream pathway genes and transcription factors are the Sonic hedgehog pathway, Smad-dependant and independent TGF b pathway, Receptor tyrosine kinase pathway, Notch pathway, and Wnt pathway. Additionally, hypoxia and inflammation, the factors of the tumour microenvironment, are also known to potentiate the epithelial to mesenchymal transition.
Fig. 2 The pathways facilitating EMT. The pathways known to induce EMT by activating the downstream pathway genes and transcription factors are the Sonic hedgehog pathway, Smad-dependant and independent TGF b pathway, Receptor tyrosine kinase pathway, Notch pathway, and Wnt pathway. Additionally, hypoxia and inflammation, the factors of the tumour microenvironment, are also known to potentiate the epithelial to mesenchymal transition.CC-BY-NC · From the PDF
Fig. 3 Schematic representation depicting the role of exosomes in the progression of EMT.
Fig. 3 Schematic representation depicting the role of exosomes in the progression of EMT.CC-BY-NC · From the PDF
Fig. 4 The consortium of EMT and MET; (A) the epithelial cells are in close association with adjacent cells and the basement membrane, through their adherent junctions; (B) loss of epithelial markers results in the dissociation of the adherent junctions, which enables the epithelial cells to acquire a hybrid epithelial/mesenchymal (E/M) phenotype (C); (D) cells attain migratory mesenchymal phenotypes upon procuring mesenchymal markers, thus depicting the phenomenon of EMT. The mesenchymal to epithelial transition (MET) is the reverse process of EMT, whereby the cells lose their mesenchymal characteristics and initially acquires partial (hybrid M/E) epithelial phenotype (E), followed by a complete epithelial phenotype (F).
Fig. 4 The consortium of EMT and MET; (A) the epithelial cells are in close association with adjacent cells and the basement membrane, through their adherent junctions; (B) loss of epithelial markers results in the dissociation of the adherent junctions, which enables the epithelial cells to acquire a hybrid epithelial/mesenchymal (E/M) phenotype (C); (D) cells attain migratory mesenchymal phenotypes upon procuring mesenchymal markers, thus depicting the phenomenon of EMT. The mesenchymal to epithelial transition (MET) is the reverse process of EMT, whereby the cells lose their mesenchymal characteristics and initially acquires partial (hybrid M/E) epithelial phenotype (E), followed by a complete epithelial phenotype (F).CC-BY-NC · From the PDF
Fig. 5 The therapeutic efficacy of exosomes in EMT.
Fig. 5 The therapeutic efficacy of exosomes in EMT.CC-BY-NC · From the PDF

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Metadata

Authors
Sen, P., Saha, M., & Ghosh, S. S.
Venue
Materials Advances
Publisher
Royal Society of Chemistry (RSC)
Published
2020
Volume
1
Issue
8
Pages
2614-2630
ISSN
2633-5409
DOI
10.1039/d0ma00455c
Cited by
21
References
2
Language
en
Licence
creativecommons.org/licenses/by-nc/3.0/ (vor, 236 d)
Funders
Department of Biotechnology, Ministry of Science and Technology (BT/PR13560/COE/34/44/2015, BT/PR25095/NER/95/1011/2017)

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