MicroRNA-98-5p inhibits proliferation and metastasis in non-small cell lung cancer by targeting TGFBR1

Jiang, Feng; Yu, Qiuhua; Chu, Ying; Zhu, Xiaobo; Lu, Wenbin; Liu, Qian; Wang, Qiang

doi:10.3892/ijo.2018.4610

Cited by 35 publications

(38 citation statements)

References 40 publications

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“…Recent published reports also shows that TGF-beta1 appear to be overproduced in COVID-19 patients [69]. Hsa-miR-9-5p, hsa-miR-98-5p and hsa-miR-23b-3p regulate TGFBR receptors during pulmonary disorders [68,70,71]. These miRNAs are part of the regulatory circuit identified in the present study and are antiviral host-miRNAs which can potentially target SARS-CoV-2 genes [10].…”

Section: Discussionsupporting

confidence: 70%

The miRNA-gene regulatory circuits in nSARS-CoV-2 and their potential correlations with pulmonary and thrombotic disorders

Khurana

Gupta

Sugadev

et al. 2020

Preprint

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In view of the worldwide spread of the novel Severe Acute Respiratory Syndrome Coronavirus 2 (nSARS-CoV-2) infection pandemic situation, research to repurpose drugs, identify novel drug targets, vaccine candidates, diagnostic markers etc have created a new race to curb the disease. To uncover nSARS-CoV-2-related important biological features and understanding the molecular basis of this disease, network biology and miRNA-gene regulatory motif-based approach is used. 11 antiviral human-microRNAs (miRNAs) which can potentially target SARS-CoV-2 genes were collated; their direct miRNA interactors were identified and a comprehensive nSARS-CoV-2 responsive miRNA:Transcription Factor (TF):gene coregulatory network was built. 1385 miRNA:TF:gene tripartite, Feed-Forward Loops (FFLs) were identified from the network. The network topology was mapped into the biological space and the overrepresented pathways were identified. Four regulatory circuits: hsa-mir-9-5p-EP300-PLCB4, hsa-mir-324-3p-MYC-HLA-F, hsa-mir-1827-E2F1-CTSV and hsa-mir-1277-5p-SP1-CANX are identified. These miRNA-gene regulatory circuits are found to regulate signalling pathways like virus endocytosis, viral replication, inflammatory response, pulmonary vascularization, cell cycle control, virus spike protein stabilization, antigen presentation, etc. Some novel computational evidences for understanding nSARS-CoV-2 molecular mechanisms controlled by these regulatory circuits is put forth. The novel associations of miRNAs and genes identified with this infection are open for experimental validation. Further, these regulatory circuits also suggest potential correlations/similarity in the molecular mechanisms during nSARS-CoV-2 infection and pulmonary diseases and thromboembolic disorders. A detailed molecular snapshot of TGF-β signalling pathway as the common mechanism that could play an important role in controlling common pathophysiology i.e. systemic inflammation, increased pulmonary pressure, ground glass opacities, D-dimer overexpression is also put forth.

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Section: Discussionsupporting

confidence: 70%

The miRNA-gene regulatory circuits in nSARS-CoV-2 and their potential correlations with pulmonary and thrombotic disorders

Khurana

Gupta

Sugadev

et al. 2020

Preprint

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“…Increasing evidence has demonstrated that numerous miRNAs are dysregulated in NScLc and that this dysregulation is a hallmark of NScLc (30)(31)(32). Recently, miRNAs have been identified as a novel player in gene regulation in NSCLC, with aberrant miRNAs expression serving pivotal roles in formation and progression of NScLc (33)(34)(35). A detailed investigation of cancer-associated miRNAs in NScLc is therefore crucial for identifying effective therapeutic targets for this disease.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Tan

Jiang

et al. 2019

Int J Mol Med

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Numerous microRNAs (miRs) are dysregulated in non-small cell lung cancer (NScLc), serving pivotal roles in its formation and progression. miR-625 is dysregulated in several types of human cancer, but its involvement in the formation and development of NScLc remains poorly understood. In the present study, we aimed to investigate miR-625 expression in NScLc and its role in regulating NScLc cell behavior. miR-625 expression in NScLc tissues and cell lines was detected using reverse transcription-quantitative polymerase chain reaction. The effects of miR-625 overexpression on NScLc cell proliferation, apoptosis, migration and invasion in vitro were assessed using an MTT assay, flow cytometry, and cell migration and invasion assays, respectively. The effects of miR-625 upregulation on NScLc growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumor-suppressing roles of miR-625 in NScLc were explored in detail. miR-625 expression was determined to be downregulated in NScLc tissues and cell lines. This decreased expression was associated with advanced clinical features and poor overall survival of patients with NScLc. Exogenous miR-625 expression suppressed NScLc cell proliferation, migration and invasion, and induced apoptosis in vitro. miR-625 upregulation hindered NScLc tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miR-625 in NScLc cells. The tumor-suppressing effects of HOXB5 silencing were similar to those of miR-625 overexpression in NScLc cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miR-625 in NScLc cells. miR-625 upregulation directly targeted HOXB5 to deactivate the Wnt/β-catenin signaling pathway in NScLc cells in vitro and in vivo. miR-625 was determined to be associated with HOXB5 suppression and Wnt/β-catenin pathway deactivation, which in turn inhibited the aggressive behavior of NScLc cells in vitro and in vivo.

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“…According to Wang et al, miR‐133a may suppress cell invasion by targeting TGFBR1 in NSCLC . Jiang et al hold the view that miR‐98‐5p inhibited proliferation and metastasis of NSCLC by targeting TGFBR1 . Recent research has suggested that TGFBR1 was activated after myocardial infarction in rats and was associated with the degree of remodeling, suggesting that TGFBR1 may be a candidate prognostic biomarker on cardiomyocyte.…”

Section: Discussionmentioning

confidence: 99%

“…25 Jiang et al hold the view that miR-98-5p inhibited proliferation and metastasis of NSCLC by targeting TGFBR1. 26 Recent research has suggested that TGFBR1 was activated after myocardial infarction in rats and was associated with the degree of remodeling, 27 suggesting that TGFBR1 may be a candidate prognostic biomarker on cardiomyocyte. Consistent with previous reports, our findings revealed that TGFBR1 was highly expressed in H/R model, and its change was decreased/increased after miR-27 mimic/inhibitor treatment.…”

Section: Downregulated Expression Of Mir-27 In Myocardial Ischemiamentioning

confidence: 99%

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Zhang

2019

The Kaohsiung J of Med Scie

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MiR‐27 prevents atherosclerosis by inhibiting inflammatory responses induced by lipoprotein lipase. Overexpression of miR‐27b attenuates angiotensin‐induced atrial fibrosis. Nevertheless, studies have rarely investigated on the effect of miR‐27 in cardiomyocyte injury. H9c2 cells were transfected with miR‐27 mimic/inhibitor. Then the cell proliferation was tested by MTT assay and the cell apoptosis was detected by flow cytometry. The luciferase activity assay was utilized to analyze the relationship between miR‐27 and TGFBR1. Quantificational real‐time polymerase chain reaction and western blot were utilized to detect the cardiomyocyte differentiation marker and nuclear factor kappa B (NF‐κB) pathway. Our outcomes demonstrated that miR‐27 expression was downregulated cardiomyocyte injury subjected to hypoxia/reoxygenation (H/R). Additionally, overexpression of miR‐27 could significantly alleviate cardiomyocyte injury by regulating cell activity and apoptosis. The luciferase activity assay confirmed that transforming growth factor ß receptor 1 (TGFBR1) is a direct hallmark of miR‐27. Besides, overexpression of miR‐27 promoted the expression of TGFBR1 in H/R model. After transfection with miR‐27 mimic/inhibitor, the expression of NF‐κB pathway‐related proteins was decreased/increased. Taken together, our data manifested that miR‐27 repressed cardiomyocyte injury induced by H/R via mediating TGFBR1 and inhibiting NF‐κB signaling pathway. Furthermore, miR‐27/ TGFBR1 might be utilized as hopeful biomarkers for myocardial ischemia diagnosis and treatment.

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MicroRNA-98-5p inhibits proliferation and metastasis in non-small cell lung cancer by targeting TGFBR1

Cited by 35 publications

References 40 publications

The miRNA-gene regulatory circuits in nSARS-CoV-2 and their potential correlations with pulmonary and thrombotic disorders

The miRNA-gene regulatory circuits in nSARS-CoV-2 and their potential correlations with pulmonary and thrombotic disorders

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

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