Melanoma is one of the most aggressive and highly resistant tumors. Cell plasticity in melanoma is one of the main culprits behind its metastatic capabilities. The detailed molecular mechanisms controlling melanoma plasticity are still not completely understood. Here we combine mathematical models of phenotypic switching with experiments on IgR39 human melanoma cells to identify possible key targets to impair phenotypic switching. Our mathematical model shows that a cancer stem cell subpopulation within the tumor prevents phenotypic switching of the other cancer cells. Experiments reveal that hsa-mir-222 is a key factor enabling this process. Our results shed new light on melanoma plasticity, providing a potential target and guidance for therapeutic studies.

MicroRNA-222 Regulates Melanoma Plasticity

Fumagalli Maria Rita;Zapperi S;
2020

Abstract

Melanoma is one of the most aggressive and highly resistant tumors. Cell plasticity in melanoma is one of the main culprits behind its metastatic capabilities. The detailed molecular mechanisms controlling melanoma plasticity are still not completely understood. Here we combine mathematical models of phenotypic switching with experiments on IgR39 human melanoma cells to identify possible key targets to impair phenotypic switching. Our mathematical model shows that a cancer stem cell subpopulation within the tumor prevents phenotypic switching of the other cancer cells. Experiments reveal that hsa-mir-222 is a key factor enabling this process. Our results shed new light on melanoma plasticity, providing a potential target and guidance for therapeutic studies.
2020
Istituto di Biofisica - IBF
Istituto di Chimica della Materia Condensata e di Tecnologie per l'Energia - ICMATE
melanoma
tumor plasticity
hsa-mir-222
reaction diffusion
kinetic equations
cancer stem cells
phenotypic switching
File in questo prodotto:
File Dimensione Formato  
prod_433266-doc_154722.pdf

accesso aperto

Descrizione: MicroRNA-222 Regulates Melanoma Plasticity
Tipologia: Versione Editoriale (PDF)
Dimensione 3.68 MB
Formato Adobe PDF
3.68 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/385884
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? 8
social impact