MiR-147b influences vascular smooth muscle cell proliferation and migration via targeting YY1 and modulating Wnt/&amp;beta;-catenin activities

Yue, Yulun; Lv, Wenyan; Zhang, Lin; Kang, Wei

doi:10.1093/abbs/gmy086

Cited by 21 publications

(9 citation statements)

References 34 publications

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“…In hydrogen peroxide‐exposed cardiomyocytes, miR‐147b suppresses cell viability and promotes cell apoptosis . Moreover, miR‐147b is involved in regulating the proliferation and migration of vascular smooth muscle cells . Notably, miR‐147b has been identified as a cancer‐related miRNA.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

Ning

Pang

Shao

et al. 2019

Clin Exp Pharma Physio

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| INTRODUC TI ONLung cancer, 85% of which is non-small-cell lung cancer (NSCLC), is the leading cause of cancer-related death in both males and females worldwide. 1 Most lung cancer patients are diagnosed at an advanced stage, and therefore have an extremely low 5-year survival rate. 2 Although great advances have been made in cancer therapeutic strategies over the past decade, the high recurrence rate still poses a high risk of decreased patient survival. 3 Therefore, elucidation of the elaborate molecular mechanism underlying NSCLC cell proliferation and metastasis is urgently needed to identify key molecular targets that can aid in the development of an effective target therapy. AbstractDeregulation of microRNAs (miRNAs) leads to malignant growth and aggressive invasion during cancer occurrence and progression. miR-147b has emerged as one of the cancer-related miRNAs that are dysregulated in multiple cancers. Yet, the relevance of miR-147b in non-small-cell lung cancer (NSCLC) remains unclear. In the present study, we aimed to report the biological function and signalling pathways mediated by miR-147b in NSCLC. Our results demonstrate that miR-147b expression is significantly downregulated in NSCLC tissues and cell lines. Overexpression of miR-147b decreased the proliferative ability, colony-forming capability, and invasive potential of NSCLC cells. Notably, our study identified ribosomal protein S15A (RPS15A), an oncogene in NSCLC, as a target gene of miR-147b. Our results showed that miR-147b negatively modulates RPS15A expression in NSCLC cells. An inverse correlation between miR-147b and RPS15A was evidenced in NSCLC specimens. Moreover, miR-147b overexpression downregulated the activation of Wnt/β-catenin signalling via targeting of RPS15A. Overexpression of RPS15A partially reversed the miR-147bmediated antitumour effect in NSCLC cells. Collectively, these findings reveal that miR-147b restricts the proliferation and invasion of NSCLC cells by inhibiting RPS15A-induced Wnt/β-catenin signalling and suggest that the miR-147b/RPS15A/ Wnt/β-catenin axis is an important regulatory mechanism for malignant progression of NSCLC. K E Y W O R D Scancer, miR-147b, non-small-cell lung cancer, ribosomal protein S15A, Wnt

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

Ning

Pang

Shao

et al. 2019

Clin Exp Pharma Physio

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“…The increase of YY1 inhibits the proliferation and migration of VSMCs cells and attenuates the effect of miRNA‐147b overexpression on the proliferation and migration of VSMCs. This study demonstrates that miRNA‐147b affects VSMC proliferation and migration by targeting YY1 and regulating Wnt/β‐catenin activity (Yue et al, ).…”

Section: Vsmc Proliferation Migration and Apoptosismentioning

confidence: 75%

“…Likewise, overexpression of miRNA‐365b‐3p directly targeted down‐regulation of ADAMTS1 and inhibited the proliferation of PDGD‐BB‐induced HVSMCs (Qu and Zhang, ). Yue et al () demonstrated that overexpression of miRNA‐147b enhanced the proliferation and migration of VSMCs and increased Wnt/β‐catenin signaling activity in VSMCs. By knocking down miRNA‐147b, it has been shown that the proliferation and migration of PDGF‐BB‐treated VSMCs or VSMCs were significantly inhibited.…”

Section: Vsmc Proliferation Migration and Apoptosismentioning

confidence: 99%

The role of microRNAs in the involvement of vascular smooth muscle cells in the development of atherosclerosis

Tang

2019

Cell Biology International

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MicroRNAs (miRNAs) are a class of nonprotein‐encoding RNAs of ~22 nucleotides in length that bind to or complement each other with a target gene messenger RNA (mRNA) to promote mRNA degradation or inhibit translation of the target mRNA. The protein required [such as Toll‐like receptor (TLR) proteins] is controlled at an optimal level. By affecting protein translation, miRNAs have become powerful regulators of biological processes, including development, differentiation, cell proliferation, and apoptosis. MiRNAs are involved in the regulation of proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMCs), thereby affecting the formation of atherosclerosis (AS). In recent years, the role and mechanism of miRNAs involved in AS development in VSMCs have been studied extensively. In the current study, the results and progress in miRNA research are reviewed.

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“…For instance, YY1 initiated the activity of the X-inactive specific transcript (Xist) promoter by directly binding to the Xist 5' region in ES cells ( 24 ). Downstream, YY1 was also revealed to be involved in the pathophysiology of AS by regulating cell proliferation and apoptosis ( 12 , 26 , 27 ). For example, a previous study reported that YY1 was involved in the promoting effects of miR-544 on the maturation and antioxidative effects of stem cell-derived endothelial-like cells ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

“…Its overexpression can cause the abnormal transcription of downstream genes, participating in disease occurrence, such as diabetes and B lymphoma ( 8 , 10 , 11 ). YY1 was reported to serve an important role in AS by mediating the proliferation and migration of VSMCs ( 12 ). In addition, a previous study indicated that YY1 was involved in the formation of foam cells in response to oxLDL ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

YY1 affects the levels and function of fibulin‑5 in ox‑LDL‑treated vascular smooth muscle cells

Wang¹,

Li²,

Cheng³

et al. 2022

Exp Ther Med

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Fibulin-5 is reportedly involved in the pathological process of atherosclerosis (AS) where low expression has been frequently observed in ruptured atherosclerotic plaques. The aim of the present study was to determine the effects of fibulin-5 on the responses of vascular smooth muscle cells (VSMC) to oxidized low-density lipoprotein (ox-LDL). The expression of fibulin-5 was studied in human aortic-VSMCs (HA-VSMCs) treated with ox-LDL. Fibulin-5 was first overexpressed by the transfection of Ov-Fibulin-5 plasmids in HA-VSMCs challenged with ox-LDL to investigate its influence on cell proliferation, migration and invasion using Cell Counting Kit-8, wound healing and Transwell assays. Yin Yang-1 (YY1) was bioinformatically predicted to bind to the promoter sites of fibulin-5, which was subsequently confirmed by dual-luciferase reporter gene assay. Fibulin-5 overexpression was able to suppress cell proliferation, invasion and migration, which was effectively reversed by YY1 silencing by the transfection of siRNA-Fibulin-5 plasmids which could induced fibulin-5 silencing. YY1 binding sites in the promoter region of fibulin-5 were identified and confirmed in vitro by chromatin immunoprecipitation assay and dual-luciferase reporter gene assay. The present results suggested that as a modulator of fibulin-5, YY1 alleviated ox-LDL-induced proliferation, invasion, migration and phenotypic transition from differentiated contractile phenotype to dedifferentiated phenotype in VSMCs. However, the mechanism underlying the YY1-mediated regulation of fibulin-5 expression needs to be confirmed further in vivo . Nevertheless, targeting fibulin-5 and YY1 could be further developed for AS therapy.

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MiR-147b influences vascular smooth muscle cell proliferation and migration via targeting YY1 and modulating Wnt/β-catenin activities

Cited by 21 publications

References 34 publications

MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

The role of microRNAs in the involvement of vascular smooth muscle cells in the development of atherosclerosis

YY1 affects the levels and function of fibulin‑5 in ox‑LDL‑treated vascular smooth muscle cells

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