Comparison of Transcriptomic Profiles of MiaPaCa-2 Pancreatic Cancer Cells Treated with Different Statins
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu srovnávací studie, časopisecké články
Grantová podpora
No. CZ.02.1.01/0.0/0.0/16_019/0000785
Operational Programme Research, Development and Education
APVV-15-0217
the Slovak Research and Development Agency
RVO-VFN64165/2021
the Czech Ministry of Health
PubMed
34207840
PubMed Central
PMC8226792
DOI
10.3390/molecules26123528
PII: molecules26123528
Knihovny.cz E-zdroje
- Klíčová slova
- DNA microarray, HMG-CoA reductase inhibitors, atorvastatin, cerivastatin, fluvastatin, pancreatic cancer, pitavastatin, pravastatin, simvastatin, statins,
- MeSH
- antitumorózní látky farmakologie MeSH
- buněčná smrt MeSH
- epigeneze genetická MeSH
- kyselina mevalonová metabolismus MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- nádory slinivky břišní farmakoterapie genetika metabolismus patologie MeSH
- pohyb buněk MeSH
- proliferace buněk MeSH
- statiny farmakologie MeSH
- transkriptom účinky léků MeSH
- výpočetní biologie metody MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- srovnávací studie MeSH
- Názvy látek
- antitumorózní látky MeSH
- kyselina mevalonová MeSH
- statiny MeSH
Statins have been widely used for the treatment of hypercholesterolemia due to their ability to inhibit HMG-CoA reductase, the rate-limiting enzyme of de novo cholesterol synthesis, via the so-called mevalonate pathway. However, their inhibitory action also causes depletion of downstream intermediates of the pathway, resulting in the pleiotropic effects of statins, including the beneficial impact in the treatment of cancer. In our study, we compared the effect of all eight existing statins on the expression of genes, the products of which are implicated in cancer inhibition and suggested the molecular mechanisms of their action in epigenetic and posttranslational regulation, and in cell-cycle arrest, death, migration, or invasion of the cancer cells.
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