MicroRNA-144-3p targets relaxin/insulin-like family peptide receptor 1 (RXFP1) expression in lung fibroblasts from patients with idiopathic pulmonary fibrosis

Bahudhanapati, Harinath; Tan, Jiangning; Dutta, Justin A.; Strock, Stephen B.; Sembrat, John; Álvarez, Diana; Rojas, Mauricio; Jäger, B; Prasse, Antje; Zhang, Yingze; Kass, Daniel J.

doi:10.1074/jbc.ra118.004910

Cited by 34 publications

(40 citation statements)

References 46 publications

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“…Relaxin 2/RXFP1 Signalling induces cell invasion via the beta-catenin pathway in endometrial cancer [44]. Expression of RXFP1 is decreased in idiopathic pulmonary fibrosis [45] and mediates the effects of miR-144-3p in lung fibroblasts from patients with idiopathic pulmonary fibrosis [46]. RXFP1 protects against airway fibrosis during homeostasis but not against fibrosis associated with chronic allergic airways disease [47].…”

Section: Discussionmentioning

confidence: 99%

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

Xie

2019

BioMed Research International

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Background and Goals. To identify a multigene signature model for prognosis of non-small-cell lung cancer (NSCLC) patients, we first found 2146 consensus differentially expressed genes (DEGs) in NSCLC overlapped in Gene Expression Omnibus (GEO) and TCGA lung adenocarcinoma (LUAD) datasets using integrated analysis. We constructed a weighted gene coexpression network (WGCN) using the consensus DEGs and identified the module significantly associated with pathological M stage and consisted of 61 genes. After univariate Cox regression analysis and subsequent stepwise model selection by the Akaike information criterion (AIC) and multivariate Cox hazard model analysis, an mRNA signature model which calculated prognostic score was generated: prognostic score = (−0.2491 × EXPRRAGB) + (−0.0679 × EXPRSPH9) + (−0.2317 × EXPRPS6KL1) + (−0.1035 × EXPRXFP1) + 0.1571 × EXPRRM2 + 0.1104 × EXPRTL1, where EXP is the fragments per kilobase million (FPKM) value of the mRNA included in the model. The prognostic model separated NSCLC patients in the TCGA-LUAD dataset into the low- and high-risk score groups with a median prognostic score of 0.972. Higher scores predicted higher risk. The area under ROC curve (AUC) was 0.994 or 0.776 in predicting the 1- to 10-year survival of NSCLC patients. The prognostic performance of this prognostic model was validated by an independent GSE11969 dataset of NSCLC adenocarcinoma with AUC values between 0.822 and 0.755 in predicting 1- to 10-year survival of NSCLC. These results suggested that the six-gene signature functioned as an independent biomarker to predict the overall survival of NSCLC adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

Xie

2019

BioMed Research International

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“…The targets of miR-133a are TGF-β receptor 1, CTGF, and collagen type 1-a1. Bahudhanapati et al reported that miR-144-3p is upregulated in IPF fibroblasts compared with the control fibroblasts [33]. miR-144-3p controls the expression of relaxin/insulin-like family peptide receptor 1(RXFP1) in fibroblasts from lungs with IPF [34].…”

Section: The Role Of Mirna In Ipfmentioning

confidence: 99%

DROSHA-Dependent miRNA and AIM2 Inflammasome Activation in Idiopathic Pulmonary Fibrosis

Cho

Lee

Stout‐Delgado

et al. 2020

IJMS

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Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease. Chronic lung inflammation is linked to the pathogenesis of IPF. DROSHA, a class 2 ribonuclease III enzyme, has an important role in the biogenesis of microRNA (miRNA). The function of miRNAs has been identified in the regulation of the target gene or protein related to inflammatory responses via degradation of mRNA or inhibition of translation. The absent-in-melanoma-2 (AIM2) inflammasome is critical for inflammatory responses against cytosolic double stranded DNA (dsDNA) from pathogen-associated molecular patterns (PAMPs) and self-DNA from danger-associated molecular patterns (DAMPs). The AIM2 inflammasome senses double strand DNA (dsDNA) and interacts with the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), which recruits pro-caspase-1 and regulates the maturation and secretion of interleukin (IL)-1β and IL-18. A recent study showed that inflammasome activation contributes to lung inflammation and fibrogenesis during IPF. In the current review, we discuss recent advances in our understanding of the DROSHA–miRNA–AIM2 inflammasome axis in the pathogenesis of IPF.

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“…It has also been reported that miR-218 regulates DN by targeting IKK-β and modulating NF-κB-mediated inflammation [24]. Moreover, miR-144 has been reported to modulate apoptosis, inflammatory factors, and fibrosis [25,26]. Nevertheless, the mechanism of miR-144 in the pathogenesis of DN remains unknown.…”

Section: Introductionmentioning

confidence: 99%

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

Min

Xie

2020

Kidney Blood Press Res

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Background: Diabetic nephropathy constitutes a large proportion of end-stage kidney failure in diabetic patients. However, the underlying molecular mechanisms remain unclear. Methods: Db/db diabetic mouse models and high glucose (HG)-induced human renal mesangial cells (HRMCs) were used as research models in vivo and in vitro. The expression of cancer susceptibility candidate 2 (CASC2) was quantified by qRT-PCR. The regulatory role of CASC2 in cell apoptosis, inflammatory factor release, and fibrosis was verified by flow cytometry, qRT-PCR, and Western blot assay, respectively. The bioinformatics prediction software DIANA and starBase v2.0 were used to predict the putative binding sites. The interactions among CASC2, miR-144, and SOCS2 were explored by the luciferase assay and Western bolt assay. Results: The expression of CASC2 in diabetic mouse models and HG-induced HRMCs was lower than that in the control (p < 0.05). Overexpression of CASC2 resulted in a decrease in the apoptosis rate, inflammatory factor release (TNF-α, IL-6, and IL-1β), expression of cleaved caspase-3, and fibrotic proteins (fibronectin, Col-IV, and TGF-β1) and an increase in Bcl-2 expression. Inhibition of CASC2 caused increased expression of miR-144. Furthermore, mechanistic investigations confirmed that activation of the miR-144/SOCS2 regulatory loop by overexpression of miR‐144 reversed the in vitro effects of CASC2 on inhibiting cell apoptosis, inflammatory factor release, and fibrosis. In addition, simultaneous overexpression of miR-144 and SOCS2 further increased the inhibition of cell apoptosis, inflammatory factor release, and fibrosis by CASC2. Conclusion: CASC2 could alleviate the degree and process of apoptosis, inflammation, and fibrosis in diabetic nephropathic models by regulating the miR-144/SOCS2 axis.

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MicroRNA-144-3p targets relaxin/insulin-like family peptide receptor 1 (RXFP1) expression in lung fibroblasts from patients with idiopathic pulmonary fibrosis

Cited by 34 publications

References 46 publications

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

A Six-Gene Signature Predicts Survival of Adenocarcinoma Type of Non-Small-Cell Lung Cancer Patients: A Comprehensive Study Based on Integrated Analysis and Weighted Gene Coexpression Network

DROSHA-Dependent miRNA and AIM2 Inflammasome Activation in Idiopathic Pulmonary Fibrosis

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

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