Involvement of MicroRNA-133a in the Development of Arteriosclerosis Obliterans of the Lower Extremities via RhoA Targeting

Li, Yongxin; Ouyang, Ming; Zhang, Shan; Ma, Jiachi; Li, Jie; Yao, Chen; Zhu, Zhou; Zhang, Longjuan; Chen, Lianzhou; Chang, Guangqi; Wang, Shenming; Wang, Wenjian

doi:10.5551/jat.27839

Cited by 12 publications

(12 citation statements)

References 27 publications

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“…qRT-PCR analyses of miR-17-5p and ETV1 expression were performed on a LightCycler 480 (Roche Diagnostics, Germany) according to our previous report [ 13 ]. The relative expression of miR-17-5p in 105 pairs of TNBC/adjacent non-tumour tissues was divided into miR-17-5p-low expression group and -high expression group according to the relative ratio of miR-17-5p expression in tumour/adjacent non-tumour tissues < or > 0.5.…”

Section: Methodsmentioning

confidence: 99%

“…The localization of miR-17-5p and ETV1 was observed by in situ hybridization (ISH) and immunohistochemistry (IHC), respectively. In situ observation of miR-17-5p was performed using 4-μm sections of samples with a digoxigenin-labelled oligonucleotide miR-17-5p detection probe (Exiqon, USA), as previously described [ 13 ]. miR-17-5p probe sequence was (5′-3′) CTACCTGCACTGTAAGCACTTTG.…”

Section: Methodsmentioning

confidence: 99%

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miR-17-5p suppresses cell proliferation and invasion by targeting ETV1 in triple-negative breast cancer

Lai

et al. 2017

BMC Cancer

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BackgroundTriple-negative breast cancer (TNBC) is the malignancy with the worst outcome among all breast cancer subtypes. We reported that ETV1 is a significant oncogene in TNBC tumourigenesis. Consequently, investigating the critical regulatory microRNAs (miRNAs) of ETV1 may be beneficial for TNBC targeted therapy.MethodsWe performed in situ hybridization (ISH) and immunohistochemistry (IHC) to detect the location of miR-17-5p and ETV1 in TNBC patient samples, respectively. miR-17-5p expression in TNBC tissues and cell lines was assessed by quantitative real-time PCR (qRT-PCR). ETV1 expression was evaluated by qRT-PCR, western blotting and IHC. Cell Counting Kit-8 (CCK-8), colony formation, Transwell and wound closure assays were utilized to determine the TNBC cell proliferation and migration capabilities. In vivo tumour metastatic assays were performed in a zebra fish model.ResultsThe abundance of miR-17-5p was significantly decreased in TNBC cell lines and clinical TNBC tissues. The miR-17-5p expression levels were closely correlated with tumour size (P < 0.05) and TNM stage (P < 0.05). By contrast, the expression of ETV1 was significantly up-regulated in TNBC cell lines and tissues. There is an inverse correlation between the expression status of miR-17-5p and ETV1 (r = −0.28, P = 3.88 × 10−3). Luciferase reporter assay confirmed that ETV1 was a direct target of miR-17-5p. Forced expression of miR-17-5p in MDA-MB-231 or BT549 cells significantly decreased ETV1 expression and suppressed cell proliferation, migration in vitro and tumour metastasis in vivo. However, rescuing the expression of ETV1 in the presence of miR-17-5p significantly recovered the cell phenotype. High miR-17-5p expression was associated with a significantly favourable prognosis, in either the ETV1-positive or ETV1-negative groups (log-rank test, P < 0.001; P < 0.001). Both univariate and multivariate analyses showed that miR-17-5p and ETV1 were independent risk factors in the prognosis of TNBC patient.ConclusionsOur data indicate that miR-17-5p acts as a tumour suppressor in TNBC by targeting ETV1, and a low-abundance of miR-17-5p may be involved in the pathogenesis of TNBC. These findings indicate that miR-17-5p may be a therapeutic target for TNBC.Electronic supplementary materialThe online version of this article (10.1186/s12885-017-3674-x) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

miR-17-5p suppresses cell proliferation and invasion by targeting ETV1 in triple-negative breast cancer

Lai

et al. 2017

BMC Cancer

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“…For example, a previous study demonstrated that miR-21 was involved in atherosclerosis by regulating the function of arterial smooth muscle cells (13). Furthermore miR-133a was shown to regulate the functions of arterial smooth muscle cells by targeting RhoA, and was involved in the pathogenesis of arterial sclerosis occlusion, which is a type of atherosclerosis affecting the lower extremities (14). In our previous study, a miRNA microarray analysis demonstrated that miR-98 was downregulated in atherosclerotic tissue (13), thus suggesting that miR-98 may be involved in the pathogenesis of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-98 rescues proliferation and alleviates ox-LDL-induced apoptosis in HUVECs by targeting LOX-1

Chen

Wang

et al. 2017

Experimental and Therapeutic Medicine

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Oxidized low-density lipoprotein (ox-LDL) is a major and critical mediator of atherosclerosis, and the underlying mechanism is thought to involve the ox-LDL-induced dysfunction of endothelial cells (ECs). MicroRNAs (miRNAs), which are a group of small non-coding RNA molecules that post-transcriptionally regulate the expression of target genes, have been associated with diverse cellular functions and the pathogenesis of various diseases, including atherosclerosis. miRNA-98 (miR-98) has been demonstrated to be involved in the regulation of cellular apoptosis; however, the role of miR-98 in ox-LDL-induced dysfunction of ECs and atherosclerosis has yet to be elucidated. Therefore, the present study aimed to investigate the role of miR-98 in ox-LDL-induced dysfunction of ECs and the underlying mechanism. It was demonstrated that miR-98 expression was markedly downregulated in ox-LDL-treated human umbilical vein ECs (HUVECs) and that miR-98 promoted the proliferation and alleviated apoptosis of HUVECs exposed to ox-LDL. In addition, the results demonstrated that lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) was a direct target of miR-98 in HUVECs, as indicated by a luciferase assay. The results of the present study suggested that miR-98 may inhibit the uptake of toxic ox-LDL, maintain HUVEC proliferation and protect HUVECs against apoptosis via the suppression of LOX-1.

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“…The abnormally expressed microRNAs identified in this study are closely associated with the pathogenesis of atherosclerosis. Based on its aberrant expression at various stages of atherosclerosis, miR-133a has been recognized to regulate the functions of artery smooth muscle cells by targeting RhoA and is involved in the pathogenesis of arterial sclerosis occlusion, a kind of atherosclerosis of the lower extremities [17].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-125b Affects Vascular Smooth Muscle Cell Function by Targeting Serum Response Factor

Chen

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidence links microRNAs to the pathogenesis of peripheral vascular disease. We recently found microRNA-125b (miR-125b) to be one of the most significantly down-regulated microRNAs in human arteries with arteriosclerosis obliterans (ASO) of the lower extremities. However, its function in the process of ASO remains unclear. This study aimed to investigate the expression, regulatory mechanisms, and functions of miR125b in the process of ASO. Methods: Using the tissue explants adherent method, vascular smooth muscle cells (VSMCs) were prepared for this study. A rat carotid artery balloon injury model was constructed to simulate the development of vascular neointima, and a lentiviral transduction system was used to overexpress serum response factor (SRF) or miR-125b. Quantitative real-time PCR (qRT-PCR) was used to detect the expression levels of miR-125b and SRF mRNA. Western blotting was performed to determine the expression levels of SRF and Ki67. In situ hybridization analysis was used to analyze the location and expression levels of miR-125b. CCK-8 and EdU assays were used to assess cell proliferation, and transwell and wound closure assays were performed to measure cell migration. Flow cytometry was used to evaluate cell apoptosis, and a dual-luciferase reporter assay was conducted to examine the effects of miR-125b on SRF. Immunohistochemistry and immunofluorescence analyses were performed to analyze the location and expression levels of SRF and Ki67. Results: miR125b expression was decreased in ASO arteries and platelet-derived growth factor (PDGF)-BB-stimulated VSMCs. miR-125b suppressed VSMC proliferation and migration but promoted VSMC apoptosis. SRF was determined to be a direct target of miR-125b. Exogenous miR-125b expression modulated SRF expression and inhibited vascular neointimal formation in ballooninjured rat carotid arteries. Conclusions: These findings demonstrate a specific role of the miR-125b/SRF pathway in regulating VSMC function and suggest that modulating miR-125b levels might be a novel approach for treating ASO.

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Involvement of MicroRNA-133a in the Development of Arteriosclerosis Obliterans of the Lower Extremities via RhoA Targeting

Cited by 12 publications

References 27 publications

miR-17-5p suppresses cell proliferation and invasion by targeting ETV1 in triple-negative breast cancer

miR-17-5p suppresses cell proliferation and invasion by targeting ETV1 in triple-negative breast cancer

MicroRNA-98 rescues proliferation and alleviates ox-LDL-induced apoptosis in HUVECs by targeting LOX-1

MicroRNA-125b Affects Vascular Smooth Muscle Cell Function by Targeting Serum Response Factor

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