LEKEŠ, Denis, Ivan SZADVÁRI, Oľga KRIŽANOVÁ, K. LOPUSNA, I. REZUCHOVA, Marie NOVÁKOVÁ, Zuzana NOVÁKOVÁ, T. PARAK and Petr BABULA. Nilotinib induces ER stress and cell death in H9c2 cells. Physiological Research. Praha: Fyziologický ústav AV ČR, 2016, vol. 65, Suppl. 4, p. "S505"-"S514", 10 pp. ISSN 0862-8408.
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Basic information
Original name Nilotinib induces ER stress and cell death in H9c2 cells
Authors LEKEŠ, Denis (703 Slovakia, belonging to the institution), Ivan SZADVÁRI (703 Slovakia, belonging to the institution), Oľga KRIŽANOVÁ (703 Slovakia, belonging to the institution), K. LOPUSNA (703 Slovakia), I. REZUCHOVA (703 Slovakia), Marie NOVÁKOVÁ (203 Czech Republic, belonging to the institution), Zuzana NOVÁKOVÁ (203 Czech Republic, belonging to the institution), T. PARAK (203 Czech Republic) and Petr BABULA (203 Czech Republic, guarantor, belonging to the institution).
Edition Physiological Research, Praha, Fyziologický ústav AV ČR, 2016, 0862-8408.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30105 Physiology
Country of publisher Czech Republic
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 1.461
RIV identification code RIV/00216224:14110/16:00092559
Organization unit Faculty of Medicine
UT WoS 000392029200011
Keywords in English Apoptosis; Cardiotoxicity; ER stress; Nilotinib; Reactive oxygen species
Tags EL OK
Tags International impact, Reviewed
Changed by Changed by: Soňa Böhmová, učo 232884. Changed: 26/4/2017 12:34.
Abstract
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 cardiotoxic and vascular effects. In this study, we focused on possible cardiotoxicity of nilotinib using H9C2 ceils as a suitable cell model. We studied rote of endoplasmic reticulum (ER) stress and apoptosis in nilotinib toxicity using a complex approach. Nilotinib 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 niiotlnib 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.
Links
MUNI/A/1365/2015, interní kód MUName: Kardiovaskulární systém: od modelu přes terapii k prevenci (Acronym: KAMOTEPRE)
Investor: Masaryk University, Category A
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