Long noncoding RNA–antisense noncoding RNA in the INK4 locus accelerates wound healing in diabetes by promoting lymphangiogenesis via regulating miR‐181a/Prox1 axis

He, Zhiyou; Wei, Tianhong; Zhang, Pihong; Zhou, Jie; Huang, Xiaoyuan

doi:10.1002/jcp.27260

Cited by 30 publications

(29 citation statements)

References 37 publications

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“…It was demonstrated in the present study that ANRIL upregulated SIRT1 by sponging miR-181a, thus identifying another ANRIL target. Remarkably, two recent investigations reinforce the present data by also documenting that ANRIL inhibits cell senescence of vascular smooth muscle cells ( 29 ) and promotes lymphangiogenesis ( 30 ) by regulating miR-181a. In conjunction with these previous studies, the present results suggested that the negative regulation of miR-181a by ANRIL may be a critical mechanism by which ANRIL exerts its versatile activities.…”

Section: Discussionsupporting

confidence: 89%

Critical role of SIRT1 upregulation on the protective effect of lncRNA ANRIL against hypoxia/reoxygenation injury in H9c2 cardiomyocytes

et al. 2021

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Dysregulation of long non-coding RNA (IncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) is associated with the risk of myocardial infarction (MI). Therefore, the present study aimed to determine the mechanisms underlying this association, which is currently poorly understood, to the best of our knowledge. The current study used an in vitro myocardial ischemia and reperfusion (MI/R) model, in which H9c2 cardiomyocytes were exposed to hypoxia/reoxygenation (H/R), which demonstrated that ANRIL expression was downregulated and that ANRIL positively regulated sirtuin 1 (SIRT1) expression following H/R injury. Subsequently, it was demonstrated that ANRIL upregulated SIRT1 expression by sponging microRNA-181a (miR-181a). In addition, ANRIL overexpression reduced lactate dehydrogenase release and apoptosis of H9c2 cardiomyocytes exposed to H/R, indicating that ANRIL prevented H/R-induced cardiomyocyte injury. Moreover, both miR-181a overexpression and SIRT1 knockdown significantly decreased the protective effects of ANRIL on H/R-induced cardiomyocyte injury, thus demonstrating that SIRT1 upregulation via sponging miR-181a is a critical mechanism that mediates the function of ANRIL. These results provided a novel mechanistic insight into the role of ANRIL in H/R-injured cardiomyocytes and suggested that the ANRIL/miR-181a/SIRT1 axis may be a therapeutic target for reducing MI/R injury.

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Section: Discussionsupporting

confidence: 89%

Critical role of SIRT1 upregulation on the protective effect of lncRNA ANRIL against hypoxia/reoxygenation injury in H9c2 cardiomyocytes

et al. 2021

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“…LncRNAs play a key role in the regulation of target genes in many diseases (Wu et al 2018, Cremer et al 2018. Furthermore, antisense lncRNAs can regulate target gene expression via a range of different mechanisms (Villegas & Zaphiropoulos 2015, He et al 2019. In the present study, our group showed that AC002454.1 may be one of the molecular targets involved in the origin of eutopic endometrial change in EMS.…”

Section: Discussionsupporting

confidence: 48%

AC002454.1 and CDK6 synergistically promote endometrial cell migration and invasion in endometriosis

Liu¹,

Wang²,

Chen³

et al. 2019

Reproduction

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Previous lncRNA microarray screening found that the AC002454.1 gene was highly expressed in endometriosis (EMS), and these expression levels were highly correlated with cyclin-dependent kinase-6 (CDK6). This study investigated the expression level and correlation between AC002454.1 and CDK6 in endometrium tissues and the influence of these changes in expression upon the biological behavior of eutopic endometrial cells. We confirmed AC002454.1 and CDK6 mRNA and protein were highly expressed in ectopic and eutopic endometrial tissue from patients with EMS and were clearly correlated. In vitro, both AC002454.1 and CDK6 positively regulated the proliferation, migration and invasion ability of eutopic endometrial cells and could promote the transformation of cells from G0/G1 phase to S phase. AC002454.1 and CDK6 may have synergistic effects, thereby affecting the biological behavior of endometrial cells, and thus promote the progression of EMS.

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“…Our results suggested that H19 could directly target miR-152-3p and repressed the expression of miR-152-3p. Many reports about the mechanism of lncRNA sponge showed that the expression of miRNA was negatively regulated after overexpression or knockdown of lncRNA (34)(35)(36), but the specific mechanism of reducing the level of miRNA by the lncRNA sponge was not described in detail. However, a previous study demonstrated that HSURs, as a noncoding RNA, could interact with miR-27 in virally transformed T cells and dramatically decreased the level of miR-27 by directing degradation of mature miR-27 in a binding-dependent manner (37).…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA H19 Promotes Tumorigenesis of Multiple Myeloma by Activating BRD4 Signaling by Targeting MicroRNA 152-3p

Jian

Guo

et al. 2020

Molecular and Cellular Biology

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Multiple myeloma (MM) accounts for over twenty percent of hematological cancer-related death worldwide. Long noncoding RNA (lncRNA) H19 is associated with multiple tumorigenesis and is increased in MM, but the underlying mechanism of H19 in MM is unclear. In this study, the expression of H19, microRNA 152-3p (miR-152-3p), and BRD4 in MM patients was evaluated by quantitative real-time PCR (qRT-PCR) and Western blotting. Colony formation and flow cytometry analysis were used to determine the effects of H19 and miR-152-3p on MM cell proliferation, apoptosis, and cell cycle. A luciferase reporter assay was conducted to confirm the interaction among H19, miR-152-3p, and BRD4. A nude mouse xenograft model was established, and the cell proliferation and apoptosis were evaluated by immunohistochemistry (IHC) staining and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling assay. We found that levels of H19 and BRD4 were upregulated and the expression of miR-152-3p was downregulated in MM patients. Dual luciferase reporter assay showed H19 targeted miR-152-3p to promote BRD4 expression. Knockdown of H19 repressed proliferation and enhanced apoptosis and cell cycle G1 arrest by upregulating miR-152-3p in MM cells. Furthermore, H19 knockdown suppressed the growth of xenograft tumor, reduced Ki-67 and BRD4 levels, and increased cell apoptosis in xenograft tumor tissues. Taking these results together, H19 knockdown suppresses MM tumorigenesis via inhibiting BRD4-mediated cell proliferation through targeting miR-152-3p, implying that H19 is a promising biomarker and drug target for MM.

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Long noncoding RNA–antisense noncoding RNA in the INK4 locus accelerates wound healing in diabetes by promoting lymphangiogenesis via regulating miR‐181a/Prox1 axis

Cited by 30 publications

References 37 publications

Critical role of SIRT1 upregulation on the protective effect of lncRNA ANRIL against hypoxia/reoxygenation injury in H9c2 cardiomyocytes

Critical role of SIRT1 upregulation on the protective effect of lncRNA ANRIL against hypoxia/reoxygenation injury in H9c2 cardiomyocytes

AC002454.1 and CDK6 synergistically promote endometrial cell migration and invasion in endometriosis

Long Noncoding RNA H19 Promotes Tumorigenesis of Multiple Myeloma by Activating BRD4 Signaling by Targeting MicroRNA 152-3p

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