Nilotinib induces ER stress and cell death in H9c2 cells
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00066087" target="_blank" >RIV/00159816:_____/16:00066087 - isvavai.cz</a>
Alternative codes found
RIV/00216224:14110/16:00092559 RIV/62157124:16370/16:43874306
Result on the web
—
DOI - Digital Object Identifier
—
Alternative languages
Result language
angličtina
Original language name
Nilotinib induces ER stress and cell death in H9c2 cells
Original language description
Tyrosine kinases inhibitors (TKi) represent a relatively novel class of anticancer drugs that target cellular pathways overexpressed in certain types of malignancies, such as chronic myeloid leukaemia (CML). Nilotinib, ponatinib and imatinib exhibit cardio toxic and vascular effects. In this study, we focused on possible cardiotoxicity of nilotinib using H9 c2 cells as a suitable cell model. We studied role of endoplasmic reticulum (ER) stress and apoptosis in nilotinib toxicity using a complex approach. Nilo tinib impaired mitochondrial function and induced formation of ROS under clinically relevant concentrations. In addition, ability of nilotinib to induce ER stress has been shown. These events result in apoptotic cell death. All these mechanisms contribute to cytotoxic effect of the drug. In addition, involvement of ER stress in nilotinib toxicity may be important in co -treatment with pharmaceuticals affecting ER and ER stress, e.g. beta -blockers or sartans, and should be further investigated.
Czech name
—
Czech description
—
Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
ED - Physiology
OECD FORD branch
—
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Physiological Research
ISSN
0862-8408
e-ISSN
—
Volume of the periodical
65
Issue of the periodical within the volume
S4
Country of publishing house
CZ - CZECH REPUBLIC
Number of pages
10
Pages from-to
"S505"-514
UT code for WoS article
000392029200011
EID of the result in the Scopus database
—