miR‑106b‑5p modulates acute pulmonary embolism via NOR1 in pulmonary artery smooth muscle cells

Chen, Heming; Ma, Qiang; Zhang, Junbo; Meng, Yan; Pan, Longfei; Tian, Hui

doi:10.3892/ijmm.2020.4532

Cited by 12 publications

(13 citation statements)

References 44 publications

(52 reference statements)

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“…Several literatures have reported NOR1 to regulate vascular cell migration and proliferation, and these important cellular processes are highly correlated with inflammation, growth factors, lipoproteins, and thrombin in vascular diseases ( Martínez-González et al, 2003 ; Rius et al, 2004 ). Importantly, these findings highlight a novel therapeutic mechanism and improve the biological understanding of the complex network modulating APE progression ( Chen et al, 2020 ).…”

Section: Mirnas Are Potential Novel Therapeutic Targets For Pementioning

confidence: 96%

The Function of microRNAs in Pulmonary Embolism: Review and Research Outlook

Luo

Shu

et al. 2021

Front. Pharmacol.

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Pulmonary embolism (PE) is a common pathologic condition that frequently occurs in patients with deep venous thrombosis. Severe PE may critically suppress cardiopulmonary function, thereby threatening the life of patients. Chronic pulmonary hypertension caused by PE may lead to deterioration of respiratory dysfunction, resulting in complete disability. MicroRNAs (miRNAs) are a group of abundantly expressed non-coding RNAs that exert multiple functions in regulating the transcriptome via post-transcriptional targeting of mRNAs. Specifically, miRNAs bind to target mRNAs in a matching mechanism between the miRNA seed sequence and mRNA 3ʹ UTR, thus modulating the transcript stability or subsequent translation activity by RNA-induced silencing complex. Current studies have reported the function of miRNAs as biomarkers of PE, revealing their mechanism, function, and targetome in venous thrombophilia. This review summarizes the literature on miRNA functions and downstream mechanisms in PE. We conclude that various related miRNAs play important roles in PE and have great potential as treatment targets. For clinical application, we propose that miRNA biomarkers combined with traditional biomarkers or miRNA signatures generated from microchips may serve as a great predictive tool for PE occurrence and prognosis. Further, therapies targeting miRNAs or their upstream/downstream molecules need to be developed more quickly to keep up with the progress of routine treatments, such as anticoagulation, thrombolysis, or surgery.

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Section: Mirnas Are Potential Novel Therapeutic Targets For Pementioning

confidence: 96%

The Function of microRNAs in Pulmonary Embolism: Review and Research Outlook

Luo

Shu

et al. 2021

Front. Pharmacol.

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“…Previous studies demonstrated that miR-106b-5p regulated the expression of PTTG1 [ 37 ], LIMK1 [ 38 ], TIMP2 [ 39 ], and NOR1 [ 40 ]. However, the relationship between miR-106b-5p and IGSF10 was not reported previously.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-106b-5p inhibits growth and progression of lung adenocarcinoma cells by downregulating IGSF10

Ling

Liao

Tang

et al. 2021

Aging

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In this study, we investigated the mechanistic role and prognostic significance of IGSF10 in lung adenocarcinoma. Oncomine database analysis showed that IGSF10 expression was significantly reduced in most cancer types, including lung adenocarcinoma (LUAD). In the TCGA-LUAD dataset, IGSF10 expression correlated positively with proportions of tumor-infiltrated B cells, CD4 + T cells, CD8 + T cells, neutrophils, macrophages, and dendritic cells. Kaplan-Meier survival analysis showed that overall survival of patients with low IGSF10 expression was significantly shorter than those with high IGSF10 expression. MiRWalk2.0 database analysis and dual luciferase reporter assays confirmed that miR-106b-5p suppressed IGSF10 expression by binding to its 3’UTR. MiR-106b-5p levels inversely correlated with IGSF10 expression in the TCGA-LUAD dataset. Moreover, inhibition of miR-106b-5p significantly decreased in vitro proliferation, migration, and invasion by LUAD cells, whereas miR-106b-5p overexpression reversed those effects. These results demonstrate that IGSF10 is an independent prognostic factor for LUAD. Furthermore, miR-106b-5p suppressed IGSF10 expression in LUAD tissues by binding to its 3’UTR, which makes IGSF10 and miR-106b-5p potential prognostic biomarkers and therapeutic targets in LUAD patients.

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“…MicroRNA 106 Suppress the migration of pulmonary artery smooth muscle cell in PAH (Chen et al, 2020).…”

Section: Hsa-mir-106b-5pmentioning

confidence: 99%

“…The mir-20a-5p-induced proliferation of pulmonary artery smooth muscle cells can exacerbate the development of PAH via targeting ATP-binding cassette subfamily A1 (Zhou et al, 2020). The mir-106b-5p played a key role in suppressing the migration of pulmonary artery smooth muscle cells, indicating that mir-106b-5p may act as a potential marker in PAH (Chen et al, 2020). These biomolecules may regulate target genes at transcriptional or posttranscriptional levels.…”

Section: Hsa-mir-106b-5pmentioning

confidence: 99%

“…Several molecular modelingbased techniques were conducted in pharmaceutical research to evaluate complex biological systems, especially for molecular docking methods, which were broadly applied in drug designs to demonstrate the ligand conformation with binding sites of target proteins. The free energy was estimated in molecular docking methods by evaluating critical phenomena that participated in the intermolecular recognition processes in ligand-receptor binding (Chen et al, 2020). Henceforth, the binding modes of drugs with target protein HSP90AA1 were screened, and the energetically stable conformations were obtained from the existing databases (Figure 5).…”

Section: Hsa-mir-106b-5pmentioning

confidence: 99%

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Molecular Characterization and Elucidation of Pathways to Identify Novel Therapeutic Targets in Pulmonary Arterial Hypertension

et al. 2021

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Background: Pulmonary arterial hypertension (PAH) is a life-threatening chronic cardiopulmonary disease. However, there are limited studies reflecting the available biomarkers from separate gene expression profiles in PAH. This study explored two microarray datasets by an integrative analysis to estimate the molecular signatures in PAH.Methods: Two microarray datasets (GSE53408 and GSE113439) were exploited to compare lung tissue transcriptomes of patients and controls with PAH and to estimate differentially expressed genes (DEGs). According to common DEGs of datasets, gene and protein overrepresentation analyses, protein–protein interactions (PPIs), DEG–transcription factor (TF) interactions, DEG–microRNA (miRNA) interactions, drug–target protein interactions, and protein subcellular localizations were conducted in this study.Results: We obtained 38 common DEGs for these two datasets. Integration of the genome transcriptome datasets with biomolecular interactions revealed hub genes (HSP90AA1, ANGPT2, HSPD1, HSPH1, TTN, SPP1, SMC4, EEA1, and DKC1), TFs (FOXC1, FOXL1, GATA2, YY1, and SRF), and miRNAs (hsa-mir-17-5p, hsa-mir-26b-5p, hsa-mir-122-5p, hsa-mir-20a-5p, and hsa-mir-106b-5p). Protein–drug interactions indicated that two compounds, namely, nedocromil and SNX-5422, affect the identification of PAH candidate biomolecules. Moreover, the molecular signatures were mostly localized in the extracellular and nuclear areas.Conclusions: In conclusion, several lung tissue-derived molecular signatures, highlighted in this study, might serve as novel evidence for elucidating the essential mechanisms of PAH. The potential drugs associated with these molecules could thus contribute to the development of diagnostic and therapeutic strategies to ameliorate PAH.

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miR‑106b‑5p modulates acute pulmonary embolism via NOR1 in pulmonary artery smooth muscle cells

Cited by 12 publications

References 44 publications

The Function of microRNAs in Pulmonary Embolism: Review and Research Outlook

The Function of microRNAs in Pulmonary Embolism: Review and Research Outlook

MicroRNA-106b-5p inhibits growth and progression of lung adenocarcinoma cells by downregulating IGSF10

Molecular Characterization and Elucidation of Pathways to Identify Novel Therapeutic Targets in Pulmonary Arterial Hypertension

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