Comprehensive Analysis of miRNA–mRNA–lncRNA Networks in Severe Asthma

Chen, Yi; Mao, Zhengdao; Shi, Yujia; Qian, Yan; Liu, Zhiguang; Xu, Yin; Zhang, Qian

doi:10.2217/epi-2018-0132

Cited by 42 publications

(31 citation statements)

References 26 publications

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“…We exhibited that HMGB2 was increased in EC and there was a positive correlation between HMGB2 and LINC00158. Subsequently, we proved that knockdown of LINC00158 repressed EC progression through inhibiting HMGB2 LINC00158 has been speculated to participate in the development of severe asthma [20]. In our present study, we observed LINC00158 was greatly increased in EC tissues compared with the normal endometrial tissues.…”

Section: Discussionsupporting

confidence: 59%

“…The rst annotation of LINC00158 also known as C21orf42 has been con rmed in the sequence of human Chromosome 21 [19]. In addition, the interactions between BCL11B-LINC00158 have been speculated to participate in the development of severe asthma [20]. By using bioinformatics tools (LncBase Predicted v.2), some microRNAs are predicted as the downstream target for LINC00158.…”

Section: Introductionmentioning

confidence: 99%

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Up-Regulation of LINC00158 Contributes to Endometrial Carcinoma Progression by Interacting with HMGB2

Cai

Hao

Chang

et al. 2020

Preprint

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Background: Increasing evidence has reported lncRNAs exhibit significant biological functions in regulating endometrial carcinoma (EC) progression. LINC00158 has been identified as a crucial modulator in various diseases. Nevertheless, the specific molecular mechanism of LINC00158 in EC remains to be investigated.Methods:q-PCR and Western blot analysis were performed to determine the expression of LINC00158 and HMGB2 in EC tissues and cells. Cell viability assay, EdU assay, flow cytometry, wound healing assay and transwell invasion assay were used to evaluate their effects on EC cell proliferation, migration and invasion. RIP assay was used to verify the interactions between LINC00158 and HMGB2. Xenograft tumor model was established to confirm the effects of LINC00158 in vivo.Results:INC00158 was obviously up-regulated in EC tissues in comparison to the normal endometrium. LINC00158 was greatly increased in EC cells than in the immortalized endometrial fibroblast cell T-HESCs. Cell viability of EC cells was reduced as indicated using CCK-8 assay and EdU experiments by knockdown of LINC00158. Loss of LINC00158 obviously induced EC cell apoptosis and blocked cell cycle, repressed EC cell migration and invasion capacity. HMGB2 was remarkably increased in EC tissues and it was positively correlated with LINC00158 expression. RIP assay was carried out and confirmed the direct binding relationship between LINC00158 and HMGB2. Decrease of LINC00158 was able to reduced HMGB2 expression in AN3CA and HEC1-A cells. LINC00158 activated HMGB2 to promote EC progression in vivo.Conclusions: Our findings implied high expression of LINC00158 promoted EC progression via interacting with HMGB2.

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Section: Discussionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Up-Regulation of LINC00158 Contributes to Endometrial Carcinoma Progression by Interacting with HMGB2

Cai

Hao

Chang

et al. 2020

Preprint

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“…The emergence of large scale comprehensive analysis of lncRNA-miRNA-mRNA networks is an important step toward understanding where lncRNAs fit into the biological processes behind cancer progression. Within the last year, these analyses have been done to further our understanding of diseases including chronic obstructive pulmonary disease, abdominal aortic aneurism, asthma, and cancer (11–14). By analyzing the differential expression of lncRNAs, miRNAs, and mRNAs, identification of key pathways and mechanisms of disease may become much clearer.…”

Section: Introductionmentioning

confidence: 99%

PVT1 Signaling Is a Mediator of Cancer Progression

et al. 2019

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There is increasing evidence that PVT1 has oncogenic properties and regulates proliferation and growth of many cancers. Themolecular mechanisms of action of PVT1 are mediated, in part, by microRNAs (miRNAs). However, some well-established transcription factors involved in cancer cell proliferation share a common thread of microRNA associations with PVT1. Furthermore, these microRNAs are also involved in mechanisms that lead to the development of drug resistance in cancer cells. While several microRNAs have been implicated directly in PVT1-mediated tumorigenesis, significant steps need to be taken to elucidate these important relationships. We synthesize the current knowledge of the miRNAs and associated genes by which PVT1 contributes to tumorigenesis. Overall, the trend suggests a negative correlation of microRNA expression with PVT1. It is clear that future studies involving PVT1 should be carried out in conjunction with microRNA analysis and should include large scale lncRNA-miRNA-mRNA network analysis. Likewise, the relationship between established transcription factors such as p53 and MYC , and processes like epithelial-mesenchymal transition may offer valuable insight into the yet unknown mechanisms of PVTI-mediated cancer progression via microRNA-dependent signaling networks.

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“…Glucocorticoid insensitivity is a serious and complicated problem in asthma (Adcock and Ito, 2004;Durham et al, 2011), mainly owing to the defective ligand to the glucocorticoid receptor, abnormal receptor nuclear translocation and abnormal combination with proinflammatory nuclear proteins (Adcock et al, 2008;Barnes and Adcock, 2009;Tonello and Poli, 2009). It has been discussed that lncRNAs, miRs and mRNAs were expressed differentially between the nonsevere glucocorticoid-sensitive asthma and severe glucocorticoid-insensitive asthma (Chen et al, 2019). We show a strong interest in the role of lncRNAs in the regulation of glucocorticoid sensitivity in asthma.…”

Section: Lncrnas Associated With Glucocorticoid Insensitivity In Asthmentioning

confidence: 81%

Long Noncoding RNAs in the Regulation of Asthma: Current Research and Clinical Implications

2020

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Asthma is a chronic airway inflammatory disorder related to variable expiratory airflow limitation, leading to wheeze, shortness of breath, chest tightness, and cough. Its characteristic features include airway inflammation, airway remodeling and airway hyperresponsiveness. The pathogenesis of asthma remains extremely complicated and the detailed mechanisms are not clarified. Long noncoding RNAs (lncRNAs) have been reported to play a prominent role in asthma and function as modulators of various aspects in pathological progress of asthma. Here, we summarize recent advances of lncRNAs in asthma pathogenesis to guide future researches, clinical treatment and drug development, including their regulatory functions in the T helper (Th) 1/Th2 imbalance, Th17/T regulatory (Treg) imbalance, eosinophils dysfunction, macrophage polarization, airway smooth muscle cells proliferation, and glucocorticoid insensitivity.

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Comprehensive Analysis of miRNA–mRNA–lncRNA Networks in Severe Asthma

Cited by 42 publications

References 26 publications

Up-Regulation of LINC00158 Contributes to Endometrial Carcinoma Progression by Interacting with HMGB2

Up-Regulation of LINC00158 Contributes to Endometrial Carcinoma Progression by Interacting with HMGB2

PVT1 Signaling Is a Mediator of Cancer Progression

Long Noncoding RNAs in the Regulation of Asthma: Current Research and Clinical Implications

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