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RNA-seq Characterization of Melanoma Phenotype Switch in 3D Collagen after p38 MAPK Inhibitor Treatment
V. Čermák, A. Škarková, L. Merta, V. Kolomazníková, V. Palušová, S. Uldrijan, D. Rösel, J. Brábek
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 2011
PubMed Central
od 2011
Europe PubMed Central
od 2011
ProQuest Central
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Health & Medicine (ProQuest)
od 2011-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2011
PubMed
33802847
DOI
10.3390/biom11030449
Knihovny.cz E-zdroje
- MeSH
- buněčná diferenciace účinky léků genetika MeSH
- fenotyp MeSH
- genová ontologie MeSH
- imidazoly farmakologie MeSH
- inhibitory proteinkinas farmakologie MeSH
- kolagen metabolismus MeSH
- lidé MeSH
- melanom genetika patologie MeSH
- mitogenem aktivované proteinkinasy p38 antagonisté a inhibitory metabolismus MeSH
- nádorové buněčné linie MeSH
- nádorové mikroprostředí účinky léků genetika MeSH
- naftaleny farmakologie MeSH
- polymerázová řetězová reakce s reverzní transkripcí MeSH
- proliferace buněk účinky léků genetika MeSH
- pyrazoly farmakologie MeSH
- pyridiny farmakologie MeSH
- regulace genové exprese u nádorů účinky léků MeSH
- sekvenování transkriptomu metody MeSH
- stanovení celkové genové exprese metody MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Melanoma phenotype plasticity underlies tumour dissemination and resistance to therapy, yet its regulation is incompletely understood. In vivo switching between a more differentiated, proliferative phenotype and a dedifferentiated, invasive phenotype is directed by the tumour microenvironment. We found that treatment of partially dedifferentiated, invasive A375M2 cells with two structurally unrelated p38 MAPK inhibitors, SB2021920 and BIRB796, induces a phenotype switch in 3D collagen, as documented by increased expression of melanocyte differentiation markers and a loss of invasive phenotype markers. The phenotype is accompanied by morphological change corresponding to amoeboid-mesenchymal transition. We performed RNA sequencing with an Illumina HiSeq platform to fully characterise transcriptome changes underlying the switch. Gene expression results obtained with RNA-seq were validated by comparing them with RT-qPCR. Transcriptomic data generated in the study will extend the present understanding of phenotype plasticity in melanoma and its contribution to invasion and metastasis.
Department of Biology Faculty of Medicine Masaryk University Kamenice 5 625 00 Brno Czech Republic
Department of Cell Biology Charles University Viničná 7 128 44 Prague Czech Republic
Citace poskytuje Crossref.org
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