Hsa_circ_0029589 knockdown inhibits the proliferation, migration and invasion of vascular smooth muscle cells via regulating miR-214-3p and STIM1

Huang, Zhen; Li, Penglei; Wu, Leiming; Zhang, Dianhong; Du, Binbin; Liang, Cui; Gao, Lu; Zhang, Yanzhou; Yao, Rui

doi:10.1016/j.lfs.2020.118251

Cited by 27 publications

(17 citation statements)

References 33 publications

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“…And ectopic STIM1 expression impaired miR-641-mdiated effects on cell proliferation and metastasis in ox-LDL-stimulated VSMCs. The evidences from our research implicated STIM1 served as a promoter in the progression of ox-LDL-stimulated VSMCs, which was proved by the existed evidences [ 43 , 44 ]. In the meantime, the above data implied that miR-641 repressed the progression of VSMCs stimulated by ox-LDL via binding to STIM1.…”

Section: Discussionsupporting

confidence: 52%

Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells

Zhang

2021

BMC Cardiovasc Disord

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Background Atherosclerosis (AS) is a primary cause of coronary heart and vascular diseases. Long non-coding RNAs (lncRNAs) are indicated to regulate AS progression. This study aimed to reveal the biological roles of lncRNA myocardial infarction associated transcript (MIAT) in oxidized low-density lipoprotein (ox-LDL)-induced human vascular smooth muscle cells (VSMCs). Methods The RNA levels of MIAT, microRNA-641 (miR-641) and stromal interaction molecule 1 (STIM1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels were determined by western blot analysis. Cell proliferation was assessed by cell colony formation and DNA content quantitation assays. Cell migration and invasion were demonstrated by wound-healing and transwell assays. The putative binding relationships between miR-641 and MIAT or STIM1 were predicted by starbase online database, and identified by dual-luciferase reporter and RNA immunoprecipitation assays. Results MIAT and STIM1 expression were substantially upregulated, whereas miR-641 expression was downregulated in ox-LDL-induced VSMCs compared with control groups. Functionally, MIAT silencing attenuated ox-LDL-induced cell proliferation, migration and invasion in VSMCs; however, these effects were impaired by miR-641 inhibitor. STIM1 overexpression also restrained miR-641-mediated impacts on cell proliferation and metastasis under ox-LDL. Mechanistically, MIAT acted as a sponge for miR-641, and miR-641 was associated with STIM1. Conclusions MIAT silencing hindered ox-LDL-induced cell proliferation, migration and invasion by downregulating STIM1 expression through binding to miR-641 in VSMCs. The mechanism provided us with a new target for AS therapy.

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Section: Discussionsupporting

confidence: 52%

Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells

Zhang

2021

BMC Cardiovasc Disord

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“…Dang et al reported that circ_0010729 repression inhibited cell proliferative and apoptotic abilities in HUVECs [ 29 ]. circ_0029589 (circ_CHFR) was unveiled to suppress cell proliferation and metastasis in vascular smooth muscle [ 30 ]. In this study, circ_CHFR was unveiled to regulate cell proliferation, apoptosis, and EndoMT in ox-LDL-induced HBMECs for the first time.…”

Section: Discussionmentioning

confidence: 99%

circ_CHFR regulates ox-LDL-mediated cell proliferation, apoptosis, and EndoMT by miR-15a-5p/EGFR axis in human brain microvessel endothelial cells

Yang

2021

Open Life Sciences

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Oxidized low-density lipoprotein (ox-LDL) is a significant risk factor for various brain vascular diseases. Circular RNA (circRNA) is involved in the pathogenesis of brain vascular diseases. This study revealed the roles of circ_CHFR in ox-LDL-mediated cell proliferation, apoptosis, and endothelial-to-mesenchymal transition (EndoMT). Our results showed that circ_CHFR and EGFR expressions were dramatically upregulated, while miR-15a-5p expression was downregulated in ox-LDL-induced human brain microvessel endothelial cells (HBMECs) relative to control groups. circ_CHFR knockdown hindered the effects of ox-LDL exposure on cell proliferation, cell cycle, apoptosis, and EndoMT in HBMECs, whereas these impacts were abolished by miR-15a-5p inhibitor. In addition, circ_CHFR functioned as a sponge of miR-15a-5p and miR-15a-5p bound to EGFR. Thus, we concluded that circ_CHFR silencing hindered ox-LDL-mediated cell proliferation, apoptosis, and EndoMT by downregulating EGFR expression through sponging miR-15a-5p in HBMECs. Our findings provide a new mechanism for studying circRNA-directed therapy in ox-LDL-induced human brain vascular diseases.

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“…ox-LDL can promote the growth, migration, and differentiation of VSMCs, leading to VSMC dysfunction (28). Studies have shown that hsa_circ_0029589 and circ_0010283 are up-regulated in ox-LDL-induced VSMCs (29)(30)(31)(32). Knockdown of these circRNAs ameliorates the dysfunction of VSMCs induced by ox-LDL and they exert these biological functions by serving as ceRNAs.…”

Section: Circrna As Cerna In Cvds Atherosclerosismentioning

confidence: 99%

Circular RNAs as Competing Endogenous RNAs in Cardiovascular and Cerebrovascular Diseases: Molecular Mechanisms and Clinical Implications

Xue

Liu

Xiong

2021

Front. Cardiovasc. Med.

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Circular RNAs (circRNAs) represent a novel class of widespread and diverse endogenous RNA molecules. This unusual class of RNA species is generated by a back-splicing event of exons or introns, resulting in a covalently closed circRNA molecule. Accumulating evidence indicates that circRNA plays an important role in the biological functions of a network of competing endogenous RNA (ceRNA). CircRNAs can competitively bind to miRNAs and abolish the suppressive effect of miRNAs on target RNAs, thus regulating gene expression at the posttranscriptional level. The role of circRNAs as ceRNAs in the pathogenesis of cardiovascular and cerebrovascular diseases (CVDs) has been recently reported and highlighted. Understanding the underlying molecular mechanism could aid the discovery of therapeutic targets or strategies against CVDs. Here, we review the progress in studying the role of circRNAs as ceRNAs in CVDs, with emphasis on the molecular mechanism, and discuss future directions and possible clinical implications.

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Hsa_circ_0029589 knockdown inhibits the proliferation, migration and invasion of vascular smooth muscle cells via regulating miR-214-3p and STIM1

Cited by 27 publications

References 33 publications

Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells

Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells

circ_CHFR regulates ox-LDL-mediated cell proliferation, apoptosis, and EndoMT by miR-15a-5p/EGFR axis in human brain microvessel endothelial cells

Circular RNAs as Competing Endogenous RNAs in Cardiovascular and Cerebrovascular Diseases: Molecular Mechanisms and Clinical Implications

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