MiR-206 Suppresses the Progression of Coronary Artery Disease by Modulating Vascular Endothelial Growth Factor (VEGF) Expression

Wang, Maojing; Yang, Jicheng; Cai, Shanglang; Ding, Wei

doi:10.12659/msm.898883

Cited by 36 publications

(19 citation statements)

References 44 publications

(43 reference statements)

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“…114 A study suggested that miR-206 might be an innovative biomarker and suppress the progression of CAD by reducing VEGF. 115 Thus, miR-206 may be a robust target for the inhibition of the growth and angiogenesis of various cancers through modulating multifaceted targets. However, further studies should be performed for understanding the mechanisms of miR-206 in angiogenesis.…”

Section: Mir-206mentioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

120

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MicroRNAs (miRNAs) are small non‐coding RNAs that regulate gene expression at a post‐transcriptional level via either the degradation or translational repression of a target mRNA. They play an irreplaceable role in angiogenesis by regulating the proliferation, differentiation, apoptosis, migration and tube formation of angiogenesis‐related cells, which are indispensable for multitudinous physiological and pathological processes, especially for the occurrence and development of vascular diseases. Imbalance between the regulation of miRNAs and angiogenesis may cause many diseases such as cancer, cardiovascular disease, aneurysm, Kawasaki disease, aortic dissection, phlebothrombosis and diabetic microvascular complication. Therefore, it is important to explore the essential role of miRNAs in angiogenesis, which might help to uncover new and effective therapeutic strategies for vascular diseases. This review focuses on the interactions between miRNAs and angiogenesis, and miRNA‐based biomarkers in the diagnosis, treatment and prognosis of angiogenesis‐related diseases, providing an update on the understanding of the clinical value of miRNAs in targeting angiogenesis.

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Section: Mir-206mentioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

120

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“…Among these miRNAs, miR-206 was identified to have protective effects on the development of coronary artery disease and cancers. 15,16 In particular, studies revealed that miR-206 participated in the progression of glioma by functioning as a tumor inhibitor to regulate cellular biological processes, and decreased miR-206 expression was associated with poor prognosis in glioma. [17][18][19] Further, miR-206 knockdown was shown to protect human embryonic stem cells (hESCs) against propofol-induced cell apoptosis, thereby inhibiting neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Wang¹,

Yang²,

Liu³

et al. 2020

OTT

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Background: Propofol has been identified to perform anti-tumor functions in glioma. However, the molecular mechanisms underlying propofol-induced prevention on migration and invasion of glioma cells remain unclear. Methods: Cell proliferation, invasion and migration were measured by 3-(4,5)-dimethylthiahiazo (−z-y1)-3,5-di-phenytetrazoliumromide assay and transwell assay, respectively. The expression of microRNA (miR)-206 and Rho-associated coiled coil-containing protein kinase 1 (ROCK1) was detected by quantitative real-time polymerase chain reaction. Western blot was used to measure the activation of the PI3K/AKT pathway. The interaction between miR-206 and ROCK1 was analyzed using the dual-luciferase reporter assay, RNA immunoprecipitation assay, and pull-down assay. Results: Propofol treatment inhibited the migration, invasion, and PI3K/AKT pathway activation in glioma cells. MiR-206 was decreased in glioma tissues and cells, while propofol exposure induced the upregulation of miR-206 in glioma cells. Besides that, we also found overexpressed miR-206 enhanced propofol-mediated inhibition on the migration, invasion, and PI3K/AKT pathway activation of glioma cells. Subsequently, ROCK1 was confirmed to be a target of miR-206. ROCK1 was elevated in glioma tissues and cells, but was reduced by propofol exposure in glioma cells. The rescue assay indicated that the miR-206/ROCK1 axis was involved in propofol-induced inhibition on the migration, invasion, and PI3K/AKT pathway activation in glioma cells. Conclusion: Propofol inhibited the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through the miR-206/ROCK1 axis, suggesting an effective clinical implication for the anesthetic to prevent the metastasis of glioma.

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“…14 In addition, miR-206 was elevated the in plasma of COPD patients and was corrected with COPD severity as measured by FEV1% predicted. 16 However, the role of miR-206 in COPD and the underlying molecular mechanisms still remain unclear. 16 However, the role of miR-206 in COPD and the underlying molecular mechanisms still remain unclear.…”

Section: Introductionmentioning

confidence: 99%

miRNA‐206 regulates human pulmonary microvascular endothelial cell apoptosis via targeting in chronic obstructive pulmonary disease

Ying

et al. 2018

J of Cellular Biochemistry

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Chronic obstructive pulmonary disease (COPD) is a leading cause of death due to tis high morbidity and mortality. microRNAs have emerged as new biomarkers for the prognosis and diagnosis of patients with COPD. In this study, we aimed to investigate the expression of microRNA‐206 (miR‐206) in lung tissues from COPD patients and to explore the regulatory role of miR‐206 in the human pulmonary microvascular endothelial cells (HPMECs). Our results showed that cigarette smoke extract (CSE) promoted cell apoptosis, increased caspase‐3 activity, and upregulated the expression of miR‐206 in HPMECs, which was significantly reversed by the miR‐206 knockdown. Transfection with miR‐206 mimics led to cell apoptosis and was closely related to changes in the protein expression levels of caspase‐3, caspase‐9, and Bcl‐2 in HPMECs. Further bioinformatics prediction analysis revealed that the 3′‐untranslated region (3′UTR) of Notch3 and vascular endothelial growth factor‐A (VEGFA) harbored miR‐206‐binding sites, and overexpression of miR‐206 repressed the luciferase activity of the vectors containing Notch3 and VEGFA 3′UTR. Overexpression of either Notch3 or VEGFA attenuated miR‐206‐induced cell apoptosis in HPMECs. More importantly, miR‐206 expression was upregulated in the lung tissues from COPD patients and was positively corrected with forced expiratory volume 1% predicted in COPD patients, while Notch3 and VEGFA mRNA levels were downregulated and were negatively correlated with the expression level of miR‐206 in the lung tissues from COPD patients. In conclusion, our results showed that miR‐206 was upregulated in COPD patients and CSE‐treated HPMECs, promoted cell apoptosis via directly targeting Notch3 and VEGFA in HPMECs.

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MiR-206 Suppresses the Progression of Coronary Artery Disease by Modulating Vascular Endothelial Growth Factor (VEGF) Expression

Cited by 36 publications

References 44 publications

The regulatory role of microRNAs in angiogenesis‐related diseases

The regulatory role of microRNAs in angiogenesis‐related diseases

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

miRNA‐206 regulates human pulmonary microvascular endothelial cell apoptosis via targeting in chronic obstructive pulmonary disease

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