Long non-coding RNA KCNQ1OT1/microRNA-204-5p/LGALS3 axis regulates myocardial ischemia/reperfusion injury in mice

Rong, Jingjing; He, Jin; Hu, Yongjun; Wang, Changlu; Fu, Qinghua; Fan, Wenjuan; Zou, Qiong-Chao; Zhang, Le; Tang, Yi; Xiang, Peng; Wang, Peng; Xiang, Yuanyuan; Peng, Jianqiang; Liu, Zhengyu; Zheng, Zhaofen

doi:10.1016/j.cellsig.2019.109441

Cited by 41 publications

(33 citation statements)

References 23 publications

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“…Huan et al found that miR-204-5p hindered GC cell proliferation, motility, and invasion [30]. Moreover, lncRNA KCNQ1OT1 could aggravate hypoxia-induced cardiac injury in vitro by targeting miR-204-5p [31]. In our results, miR-204-5p was remarkably reduced in GC cells under hypoxia.…”

Section: Discussionsupporting

confidence: 64%

Silencing circSLAMF6 represses cell glycolysis, migration, and invasion by regulating the miR-204-5p/MYH9 axis in gastric cancer under hypoxia

et al. 2020

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Background: Gastric cancer (GC) is a malignant tumor of the digestive tract. Hypoxia plays an important role in the development of cancer, including GC. The present study aimed to investigate the role of circular RNA SLAMF6 (circSLAMF6) in the progression of GC under hypoxia. Methods: The expression of circSLAMF6, microRNA-204-5p (miR-204-5p) and myosin heavy chain 9 (MYH9) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). GC cells were maintained under hypoxia (1% O2) for experiments in vitro. Glucose consumption and lactate production were determined by a Glucose Assay Kit and a Lactate Assay Kit, respectively. Levels of all protein were detected by Western blot. Cell migration and invasion were examined by Transwell assay. The interaction between miR-204-5p and circSLAMF6 or MYH9 was analyzed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Murine xenograft model was established to explore the role of circSLAMF6 in vivo. Results: CircSLAMF6 expression was increased in GC cells under hypoxia. Hypoxia promoted glycolysis, migration, and invasion in GC cells, which were reversed by circSLAMF6 knockdown. CircSLAMF6 was validated as a miR-204-5p sponge, and MYH9 was a target of miR-204-5p. Functionally, miR-204-5p inhibitor weakened the inhibition of circSLAMF6 knockdown on GC cell progression under hypoxia. Besides, MYH9 depletion suppressed glycolysis, migration, and invasion in GC cells under hypoxia. Importantly, circSLAMF6 deficiency inhibited tumor growth in vivo by regulating the miR-204-5p/MYH9 axis. Conclusion: CircSLAMF6 was involved in glycolysis, migration, and invasion by regulating the miR-204-5p/MYH9 axis in GC cells under hypoxia.

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Section: Discussionsupporting

confidence: 64%

Silencing circSLAMF6 represses cell glycolysis, migration, and invasion by regulating the miR-204-5p/MYH9 axis in gastric cancer under hypoxia

et al. 2020

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“…Downregulation of hypoxia inducible factor 1 α -antisense RNA 1 (HIF1A-AS1) and upregulation of miR-204 inhibited myocardial cell apoptosis to mitigate ventricular remodeling and ameliorate cardiac function in a myocardial IRI mouse model via regulating SOCS2 (Suppressor of cytokine signaling 2) [ 46 ]. Downregulation of the lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) resulted in the reduction of the apoptosis rate of myocardial tissues and the alleviation of myocardial IRI in mouse models through the miR-204-5p/LGALS3 axis [ 47 ]. Downregulation of the lncRNA maternally expressed gene 3 (MEG3) protected myocardial cells against I/R-induced apoptosis through the miR-7-5p/PARP1 pathway [ 48 ].…”

Section: Lncrna/circrna-mirna-mrna Axis In Irimentioning

confidence: 99%

Long Noncoding RNA/Circular RNA-miRNA-mRNA Axes in Ischemia-Reperfusion Injury

Gong

Zhou

Lai

et al. 2020

BioMed Research International

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Ischemia-reperfusion injury (IRI) elicits tissue injury involved in a wide range of pathologies. Multiple studies have demonstrated that noncoding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs), participate in the pathological development of IRI, and they may act as biomarkers, therapeutic targets, or prognostic indicators. Nonetheless, the specific molecular mechanisms of ncRNAs in IRI have not been completely elucidated. Regulatory networks among lncRNAs/circRNAs, miRNAs, and mRNAs have been the focus of attention in recent years. Studies on the underlying molecular mechanisms have contributed to the discovery of therapeutic targets or strategies in IRI. In this review, we comprehensively summarize the current research on the lncRNA/circRNA-miRNA-mRNA axes and highlight the important role of these axes in IRI.

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“…Increased kcnq1ot1 levels are observed in peripheral blood monocyte cells isolated from patients with coronary artery disease 12 . Importantly, silencing of kcnq1ot1 has been shown to mitigate myocardial ischemia/reperfusion injury 13 . It is still unclear, however, whether kcnq1ot1 is involved in the development of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis

Deng

Chen

et al. 2020

Cell Death Dis

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Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE−/− mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE−/− mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.

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Long non-coding RNA KCNQ1OT1/microRNA-204-5p/LGALS3 axis regulates myocardial ischemia/reperfusion injury in mice

Cited by 41 publications

References 23 publications

Silencing circSLAMF6 represses cell glycolysis, migration, and invasion by regulating the miR-204-5p/MYH9 axis in gastric cancer under hypoxia

Silencing circSLAMF6 represses cell glycolysis, migration, and invasion by regulating the miR-204-5p/MYH9 axis in gastric cancer under hypoxia

Long Noncoding RNA/Circular RNA-miRNA-mRNA Axes in Ischemia-Reperfusion Injury

LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis

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