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Trichostatin A inhibits rhabdomyosarcoma proliferation and induces differentiation through MyomiR reactivation
M. Tarnowski, M. Tkacz, P. Kopytko, J. Bujak, K. Piotrowska, A. Pawlik
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články
NLK
Free Medical Journals
od 2000
Freely Accessible Science Journals
od 2000
ProQuest Central
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
- MeSH
- acetylace účinky léků MeSH
- apoptóza účinky léků MeSH
- buněčná diferenciace účinky léků MeSH
- epigeneze genetická účinky léků genetika MeSH
- inhibitory histondeacetylas farmakologie MeSH
- kyseliny hydroxamové farmakologie MeSH
- lidé MeSH
- mikro RNA metabolismus MeSH
- nádorové buněčné linie MeSH
- proliferace buněk účinky léků MeSH
- rhabdomyosarkom metabolismus MeSH
- vývoj svalů účinky léků genetika MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
Rhabdomyosarcoma (RMS) is a malignant tumour of soft tissues, occurring mainly in children and young adults. RMS cells derive from muscle cells, which due to mutations and epigenetic modifications have lost their ability to differentiate. Epigenetic modifications regulate expression of genes responsible for cell proliferation, maturation, differentiation and apoptosis. HDAC inhibitors suppress histone acetylation; therefore, they are a promising tool used in cancer therapy. Trichostatin A (TsA) is a pan-inhibitor of HDAC. In our study, we investigated the effect of TsA on RMS cell biology. Our findings strongly suggest that TsA inhibits RMS cell proliferation, induces cell apoptosis, and reactivates tumour cell differentiation. TsA up-regulates miR-27b expression, which is involved in the process of myogenesis. Moreover, TsA increases susceptibility of RMS cells to routinely used chemotherapeutics. In conclusion, TsA exhibits anti-cancer properties, triggers differentiation, and thereby can complement an existing spectrum of chemotherapeutics used in RMS therapy.
Literatura
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- $a Rhabdomyosarcoma (RMS) is a malignant tumour of soft tissues, occurring mainly in children and young adults. RMS cells derive from muscle cells, which due to mutations and epigenetic modifications have lost their ability to differentiate. Epigenetic modifications regulate expression of genes responsible for cell proliferation, maturation, differentiation and apoptosis. HDAC inhibitors suppress histone acetylation; therefore, they are a promising tool used in cancer therapy. Trichostatin A (TsA) is a pan-inhibitor of HDAC. In our study, we investigated the effect of TsA on RMS cell biology. Our findings strongly suggest that TsA inhibits RMS cell proliferation, induces cell apoptosis, and reactivates tumour cell differentiation. TsA up-regulates miR-27b expression, which is involved in the process of myogenesis. Moreover, TsA increases susceptibility of RMS cells to routinely used chemotherapeutics. In conclusion, TsA exhibits anti-cancer properties, triggers differentiation, and thereby can complement an existing spectrum of chemotherapeutics used in RMS therapy.
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