Long noncoding RNA PVT1 contributes to vascular endothelial cell proliferation via inhibition of miR‑190a‑5p in diagnostic biomarker evaluation of chronic heart failure

Sun, Bin; Meng, Meng; Wei, Jiali; Wang, Shuguang

doi:10.3892/etm.2020.8599

Cited by 27 publications

(19 citation statements)

References 37 publications

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“…In our study, we first observed a significant decrease in survival rate of hypoxicinduced cardiomyocytes and a significant increase in apoptosis rate, suggesting that PVT1 may be related to hypoxia-induced cardiomyocyte injury. In the study of Sun et al [18], PVT1 was highly expressed in patients with heart failure, which was in line with our results. Then, for the purpose of further analyzing PVT1's effect on hypoxia-induced cardiomyocytes, we knocked down PVT1.…”

Section: Discussionsupporting

confidence: 93%

LncRNA PVT1 Promotes Hypoxia-Induced Cardiomyocyte Injury by Inhibiting miR-214-3p

Liu

Zhang

Lun³

et al. 2021

BioMed Research International

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Objective. To explore the effect and related mechanism of LncRNA PVT1 on hypoxia-induced cardiomyocyte injury. Methods. PVT1RNA and miR-214-3p levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell vitality and apoptosis were, respectively, evaluated by Cell Counting Kit-8 (CCK-8) and flow cytometry analysis. Starbase and Dual luciferase reporter (DLR) gene assay was employed to validate the interaction between miR-214-3p and PVT1. Results. PVT1 was statistically upregulated, and miR-214-3p was statistically downregulated in hypoxia-induced H9c2 cells. The survival rate of H9c2 cells induced by hypoxia decreased statistically, while the apoptosis rate increased statistically ( P < 0.05 ). PVT1 knockdown upregulated the hypoxia-induced H9c2 cell viability and inhibited apoptosis. DLR assay verified the targeting relationship between PVT1 and miR-214-3p. In addition, miR-214-3p inhibitors reversed the viability of H9c2 cells with PVT1 knockout and promoted apoptosis. Conclusion. Silencing PVT1 can enhance the hypoxia-induced H9c2 cell viability and inhibit apoptosis, providing a potential target for the treatment of cardiovascular diseases.

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Section: Discussionsupporting

confidence: 93%

LncRNA PVT1 Promotes Hypoxia-Induced Cardiomyocyte Injury by Inhibiting miR-214-3p

Liu

Zhang

Lun³

et al. 2021

BioMed Research International

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“…LncRNA is characterized with more than 200 nucleotides while miRNA is about 22 nucleotides in length. 4 LncRNA and miRNA are involved in various cellular processes, including cell division, invasion and survival. 5 Dysregulation of lncRNA or miRNA usually causes tumor initiation and progression.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

Du¹,

Liu²,

Tian³

et al. 2020

CMAR

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Background: Glioma is one of the leading causes of cancer-related deaths. This study aimed to investigate the function and mechanism of long noncoding RNA (lncRNA) LINC00173 in the regulation of glioma progression. Methods: LINC00173 expression was measured using qRT-PCR. Survival rate was analyzed through Kaplan-Meier method. CCK8, colony formation and EdU assays were performed to measure cell proliferation while transwell was used to determine cell migration and invasion. Luciferase reporter assay was conducted to test RNA interaction. Results: LINC00173 expression was elevated in glioma tissues and cells. LINC00173 high expression predicted poor prognosis. Loss of LINC00173 inhibited proliferation, migration and invasion. LINC00173 interacted with miR-765 to enhance NUTF2 expression. MiR-765 expression was negatively correlated with LINC00173 and NUTF2 in glioma tissues. NUTF2 level was increased in glioma tissues. NUTF2 overexpression rescued the potential of proliferation, migration and invasion in LINC00173-silenced cells. Conclusion: Our research demonstrated that LINC00173 promotes glioma progression through targeting miR-765/NUTF2 axis.

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“…PVT1 proliferates vascular endothelial cells by directly decreasing the expression of miR-190a-5p and serves as an effective diagnostic biomarker in the chronic heart failure. [ 41 ] PVT1 positively regulates cardiac hypertrophy and shown an upregulation of 2.5 fold in hypertrophic hearts after transverse aortic constriction for four weeks. [ 42 ] PVT1 was also shown regulates atrial fibrosis, commonly associated with congestive heart failure, by acting as a sponge for miR-128-3p.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA plasmacytoma variant translocation 1 linked to hypoxia-induced cardiomyocyte injury of H9c2 cells by targeting miR-135a-5p/forkhead box O1 axis

Zheng

Wang

et al. 2020

Chinese Medical Journal

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Background Myocardial infarction occurs due to insufficient (ischemia) blood supply to heart for long time; plasmacytoma variant translocation 1 (PVT1) is a long non-coding RNAs (lncRNAs) involved in the pathogenesis of various diseases, including heart disease; However, few studies have explored its role. The present study evaluated the effects of lncRNA PVT1 on hypoxic rat H9c2 cells. Methods Hypoxic injury was examined by measuring cell viability and apoptosis by using cell counting kit-8 activity and flow cytometry assays. Gene expressions after hypoxia were estimated by quantitative real time polymerase chain reaction and the signaling pathway were explored by Western blot analysis. RNA immunoprecipitation and luciferase reporter assays were applied to examine the interactions among genes. Data were analyzed using t -test with one-way or two-way analysis of variance. Results The lncRNA PVT1 is up-regulated in hypoxia-stressed H9c2 cells and knockdown of PVT1 mitigates hypoxia-induced injury in H9c2 cells. PVT1 acts as a sponge for miR-135a-5p and knockdown of PVT1 attenuated the increased hypoxia-induced injury by up-regulating miR-135a-5p. Forkhead box O1 ( FOXO1 ) was identified as a target of miR-135a-5p, and the expression was negatively regulated by miR-135a-5p. The exploration of the underlying mechanism demonstrated that knockdown of FOXO1 reversed PVT1/miR-135a-5p mediated hypoxia-induced injury in H9c2 cells. Conclusions PVT1 plays a crucial role in hypoxia-injured H9c2 cells through sponging miR-135a-5p and then positively regulating FOXO1 .

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Long noncoding RNA PVT1 contributes to vascular endothelial cell proliferation via inhibition of miR‑190a‑5p in diagnostic biomarker evaluation of chronic heart failure

Cited by 27 publications

References 37 publications

LncRNA PVT1 Promotes Hypoxia-Induced Cardiomyocyte Injury by Inhibiting miR-214-3p

LncRNA PVT1 Promotes Hypoxia-Induced Cardiomyocyte Injury by Inhibiting miR-214-3p

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

Long non-coding RNA plasmacytoma variant translocation 1 linked to hypoxia-induced cardiomyocyte injury of H9c2 cells by targeting miR-135a-5p/forkhead box O1 axis

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