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Circ_0004214 prevents human cardiomyocytes from doxorubicin induced cardiotoxicity by governing the miR-22-3p/GATA4 pathway

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Title Circ_0004214 prevents human cardiomyocytes from doxorubicin induced cardiotoxicity by governing the miR-22-3p/GATA4 pathway
 
Creator Yang, Lin
Liu, Ya Nan
Gu, Yi
Zhu, Lan
Guo, Qi
 
Subject Anticancer
circular RNAs
GATA binding protein
microRNA
Reactive oxygen species (ROS)
 
Description 622-629
In a clinical setting, the likelihood of doxorubicin (DOX) causing cardiotoxicity is high. However, the underlying
mechanism remains obscure. In this study, we investigated whether DOX toxicity is associated with the deregulation of
circular RNA_0004212 (circ_0004214). Circ_0004214, microRNA-22-3p (miR-22-3p), and GATA binding protein 4
(GATA4) expression in human cardiomyocyte AC16 cells was detected via RT-qPCR. Lactate dehydrogenase (LDH)
release, reactive oxygen species (ROS) production, malondialdehyde (MDA) content, and 4-hydroxynonenal (4-HNE)
content were assessed using corresponding commercial kits. Cell viability and apoptosis were analyzed using cell counting
kit-8 (CCK-8) and flow cytometry assays. Western blot assay was used to evaluate apoptosis-related markers and GATA4
protein levels. Dual-luciferase reporter validated the relationship between miR-22-3p and circ_0004214 or GATA4.
Declined circ_0004214 was viewed in DOX-treated AC16 cells. DOX treatment weakened cell viability, and promoted
oxidative stress and apoptosis, which was ameliorated via circ_0004214 overexpression. In addition, circ_0004214
promoted GATA4 expression by decoying miR-22-3p. Overall, the results have demonstrated that circ_0004214 protects
against DOX-induced cardiotoxicity via governing miR-22-3p/GATA4 pathway, and thereby reveal promising therapeutic
strategies against cardiotoxicity.
 
Date 2023-07-31T10:02:17Z
2023-07-31T10:02:17Z
2023-07
 
Type Article
 
Identifier 0975-1009 (Online); 0019-5189 (Print)
http://nopr.niscpr.res.in/handle/123456789/62382
https://doi.org/10.56042/ijeb.v61i08.3674
 
Language en
 
Publisher NIScPR-CSIR,India
 
Source IJEB Vol.61(08) [August 2023]