circRNA CDR1as Promotes Pulmonary Artery Smooth Muscle Cell Calcification by Upregulating CAMK2D and CNN3 via Sponging miR-7-5p

Ma, Cui; Gu, Rui; Wang, Xiaoying; He, Siyu; Bai, June; Zhang, Lixin; Zhang, Junting; Li, Qian; Qu, Lihui; Wei, Xin; Jiang, Yuan; Li, Fēi; Zhao, Xin; Zhu, Daling

doi:10.1016/j.omtn.2020.09.018

Cited by 48 publications

(39 citation statements)

References 47 publications

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“…In precent study, E2F2 expression was possibly modulated via lncRNA FAM87A-hsa-miR-31-5p/hsa-miR-7-5p in human aortic dissection tissue. Recent study investigated the implication overexpression miR-7-5p, finding that miR-7-5p agomir transfection markedly suppressed mineralization of pulmonary artery smooth muscle cell matrix under hypoxic conditions [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Integrated analysis of lncRNA-miRNA-mRNA ceRNA network in human aortic dissection

Zhang

Bian

et al. 2021

BMC Genomics

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Background Many studies on long chain non-coding RNAs (lncRNAs) are published in recent years. But the roles of lncRNAs in aortic dissection (AD) are still unclear and should be further examined. The present work focused on determining the molecular mechanisms underlying lncRNAs regulation in aortic dissection on the basis of the lncRNA-miRNA-mRNA competing endogenous RNA (ceRNA) network. Methods This study collected the lncRNAs (GSE52093), mRNAs (GSE52093) and miRNAs (GSE92427) expression data within human tissue samples with aortic dissection group and normal group based on Gene Expression Omnibus (GEO) database. Results This study identified three differentially expressed lncRNAs (DELs), 19 differentially expressed miRNAs (DEmiRs) and 1046 differentially expressed mRNAs (DEGs) identified regarding aortic dissection. Furthermore, we constructed a lncRNA-miRNA-mRNA network through three lncRNAs (including two with up-regulation and one with down-regulation), five miRNAs (five with up-regulation), as well as 211 mRNAs (including 103 with up-regulation and 108 with down-regulation). Simultaneously, we conducted functional enrichment and pathway analyses on genes within the as-constructed ceRNA network. According to our PPI/ceRNA network and functional enrichment analysis results, four critical genes were found (E2F2, IGF1R, BDNF and PPP2R1B). In addition, E2F2 level was possibly modulated via lncRNA FAM87A-hsa-miR-31-5p/hsa-miR-7-5p or lncRNA C9orf106-hsa-miR-7-5p. The expression of IGF1R may be regulated by lncRNA FAM87A-hsa-miR-16-5p/hsa-miR-7-5p or lncRNA C9orf106-hsa-miR-7-5p. Conclusion In conclusion, the ceRNA interaction axis we identified is a potentially critical target for treating AD. Our results shed more lights on the possible pathogenic mechanism in AD using a lncRNA-associated ceRNA network.

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Section: Discussionmentioning

confidence: 99%

Integrated analysis of lncRNA-miRNA-mRNA ceRNA network in human aortic dissection

Zhang

Bian

et al. 2021

BMC Genomics

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“…At present, we demonstrated CAMK2D was a functional downstream target of miR-135b. CAMK2D is a novel tumor suppressor, which has been found to be inactivated in several types of cancers, including colorectal cancer, prostate cancer, and lung cancer [35][36][37]. CAMK2D was frequently decreased in colorectal cancer and was associated with poor prognosis [38].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-135b/CAMK2D Axis Contribute to Malignant Progression of Gastric Cancer through EMT Process Remodeling

Huangfu¹,

He²,

Han³

et al. 2021

Int. J. Biol. Sci.

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There is a continued need for investigating the roles of microRNAs (miRNAs) and their targets on the progression of gastric cancer (GC), especially metastasis. Here, we performed an integrated study to identify dysregulated miRNAs critical for GC development and progression. miR-135b was determined as a promising biomarker for GC. The expression level of miR-135b was increased among GC cell lines, patient tumor tissues, serum samples, and correlation with aggravation of the GC patients. The in vitro functional assays demonstrated overexpression of miR-135b promoted cell proliferation, migration and invasion in GC, while miR-135b inhibition led to the opposite results. CAMK2D was found to be the direct target of miR-135b, serving as a tumor suppressor in GC cells. Based on our and public datasets, we confirmed the attenuation of CAMK2D expression in GC tissues. And, the expression levels of miR-135b and CAMK2D were closely associated with prognosis of GC patients. Ectopic expression of miR-135b resulted in the down-regulation of CAMK2D. Additionally, CAMK2D was a prerequisite for miR-135b to promote GC cells proliferation and migration by regulating the EMT process, which was confirmed by the in vivo experiments. Importantly, in vivo injection of miR-135b antagomir significantly repressed the tumor growth and metastasis of xenograft models, which suggested that the miR-135b antagomir were promising for clinical applications. Taken together, these results indicate that miR-135b/CAMK2D axis drives GC progression by EMT process remodeling, suggesting that miR-135b may be utilized as a new therapeutic target and prognostic marker for GC patients.

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“…CNN3 binds to F-actin and is essential for cytoskeletal rearrangement and wound healing ( Daimon et al, 2013 ; Ciuba et al, 2018 ). CNN3 is highly expressed in the brain ( Junghans and Herzog, 2018 ), cancers ( Hong et al, 2019 ; Nair et al, 2019 ; Xia et al, 2020 ), smooth muscle ( Ma et al, 2020 ), and human placenta cytotrophoblasts ( Shibukawa et al, 2010 ; Appel et al, 2014 ). High-throughput transcriptomic analysis in patients with hematological malignancies revealed that CNN3 expression can be used as a marker of systemic inflammatory response syndrome or sepsis ( Labiad et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Knockdown of CNN3 Impairs Myoblast Proliferation, Differentiation, and Protein Synthesis via the mTOR Pathway

She

Jiang

et al. 2021

Front. Physiol.

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BackgroundMyogenesis is a complex process that requires optimal outside–in substrate–cell signaling. Calponin 3 (CNN3) plays an important role in regulating myogenic differentiation and muscle regeneration; however, the precise function of CNN3 in myogenesis regulation remains poorly understood. Here, we investigated the role of CNN3 in a knockdown model in the mouse muscle cell line C2C12.MethodsMyoblast proliferation, migration, differentiation, fusion, and protein synthesis were examined in CNN3 knockdown C2C12 mouse muscle cells. Involvement of the mTOR pathway in CNN3 signaling was explored by treating cells with the mTOR activator MHY1485. The regulatory mechanisms of CNN3 in myogenesis were further examined by RNA sequencing and subsequent gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA).ResultsDuring proliferation, CNN3 knockdown caused a decrease in cell proliferation and migration. During differentiation, CNN3 knockdown inhibited myogenic differentiation, fusion, and protein synthesis in C2C12 cells via the AKT/mTOR and AMPK/mTOR pathways; this effect was reversed by MHY1485 treatment. Finally, KEGG and GSEA indicated that the NOD-like receptor signaling pathway is affected in CNN3 knockdown cell lines.ConclusionCNN3 may promote C2C12 cell growth by regulating AKT/mTOR and AMPK/mTOR signaling. The KEGG and GSEA indicated that inhibiting CNN3 may activate several pathways, including the NOD-like receptor pathway and pathways involved in necroptosis, apoptosis, and inflammation.

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circRNA CDR1as Promotes Pulmonary Artery Smooth Muscle Cell Calcification by Upregulating CAMK2D and CNN3 via Sponging miR-7-5p

Cited by 48 publications

References 47 publications

Integrated analysis of lncRNA-miRNA-mRNA ceRNA network in human aortic dissection

Integrated analysis of lncRNA-miRNA-mRNA ceRNA network in human aortic dissection

MicroRNA-135b/CAMK2D Axis Contribute to Malignant Progression of Gastric Cancer through EMT Process Remodeling

Knockdown of CNN3 Impairs Myoblast Proliferation, Differentiation, and Protein Synthesis via the mTOR Pathway

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