Microrna-222 regulates melanoma plasticity

Maria Chiara Lionetti; Filippo Cola; Oleksandr Chepizhko; Maria Rita Fumagalli; Francesc Font-Clos; Roberto Ravasio; Saverio Minucci; Paola Canzano; Marina Camera; Guido Tiana; Stefano Zapperi; Caterina A.M. La Porta

doi:10.3390/jcm9082573

Microrna-222 regulates melanoma plasticity

Maria Chiara Lionetti, Filippo Cola, Oleksandr Chepizhko, Maria Rita Fumagalli, Francesc Font-Clos, Roberto Ravasio, Saverio Minucci, Paola Canzano, Marina Camera, Guido Tiana, Stefano Zapperi, Caterina A.M. La Porta

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Article number	2573
Pages (from-to)	1-20
Number of pages	20
Journal	Journal of Clinical Medicine
Volume	9
Issue number	8
DOIs	https://doi.org/10.3390/jcm9082573
Publication status	Published - Aug 2020

Keywords

Cancer stem cells
Hsa-mir-222
Kinetic equations
Melanoma
Phenotypic switching
Reaction diffusion
Tumor plasticity

ASJC Scopus subject areas

Medicine(all)

Access to Document

10.3390/jcm9082573

Cite this

@article{21f41eebe942491aa1b5a46470cf6996,

title = "Microrna-222 regulates melanoma plasticity",

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.",

keywords = "Cancer stem cells, Hsa-mir-222, Kinetic equations, Melanoma, Phenotypic switching, Reaction diffusion, Tumor plasticity",

author = "Lionetti, {Maria Chiara} and Filippo Cola and Oleksandr Chepizhko and Fumagalli, {Maria Rita} and Francesc Font-Clos and Roberto Ravasio and Saverio Minucci and Paola Canzano and Marina Camera and Guido Tiana and Stefano Zapperi and {La Porta}, {Caterina A.M.}",

note = "Publisher Copyright: {\textcopyright} 2020 by the authors. Licensee MDPI, Basel, Switzerland.",

year = "2020",

month = aug,

doi = "10.3390/jcm9082573",

language = "English",

volume = "9",

pages = "1--20",

journal = "Journal of Clinical Medicine",

issn = "2077-0383",

publisher = "MDPI AG",

number = "8",

}

TY - JOUR

T1 - Microrna-222 regulates melanoma plasticity

AU - Lionetti, Maria Chiara

AU - Cola, Filippo

AU - Chepizhko, Oleksandr

AU - Fumagalli, Maria Rita

AU - Font-Clos, Francesc

AU - Ravasio, Roberto

AU - Minucci, Saverio

AU - Canzano, Paola

AU - Camera, Marina

AU - Tiana, Guido

AU - Zapperi, Stefano

AU - La Porta, Caterina A.M.

PY - 2020/8

Y1 - 2020/8

N2 - 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.

AB - 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.

KW - Cancer stem cells

KW - Hsa-mir-222

KW - Kinetic equations

KW - Melanoma

KW - Phenotypic switching

KW - Reaction diffusion

KW - Tumor plasticity

UR - http://www.scopus.com/inward/record.url?scp=85101162802&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85101162802&partnerID=8YFLogxK

U2 - 10.3390/jcm9082573

DO - 10.3390/jcm9082573

M3 - Article

AN - SCOPUS:85101162802

SN - 2077-0383

VL - 9

SP - 1

EP - 20

JO - Journal of Clinical Medicine

JF - Journal of Clinical Medicine

IS - 8

M1 - 2573

ER -

Microrna-222 regulates melanoma plasticity

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this