The topological key lncRNA H2k2 from the ceRNA network promotes mesangial cell proliferation in diabetic nephropathy<i>via</i>the miR‐449a/b/Trim11/Mek signaling pathway

Chen, Wenyun; Peng, Rui; Sun, Yan; Liu, Handeng; Zhang, Luyu; Peng, Huimin; Zhang, Zheng

doi:10.1096/fj.201900522r

Cited by 32 publications

(24 citation statements)

References 43 publications

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“…Many studies have reported that lncRNAs participate in DN through regulating target gene expression 20,21 . For example, silencing of the lncRNA XIST contributed to preventing renal interstitial fibrosis in DN 22 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA ARAP1‐AS2 promotes high glucose‐induced human proximal tubular cell injury via persistent transactivation of the EGFR by interacting with ARAP1

Tian

et al. 2020

J Cellular Molecular Medi

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The persistent transactivation of epidermal growth factor receptor (EGFR) causes subsequent activation of the TGF‐β/Smad3 pathway, which is closely associated with fibrosis and cell proliferation in diabetic nephropathy (DN), but the exact mechanism of persistent EGFR transactivation in DN remains unclear. ARAP1, a susceptibility gene for type 2 diabetes, can regulate the endocytosis and ubiquitination of membrane receptors, but the effect of ARAP1 and its natural antisense long non‐coding RNA (lncRNA), ARAP1‐AS2, on the ubiquitination of EGFR in DN is not clear. In this study, we verified that the expression of ARAP1 and ARAP1‐AS2 was significantly up‐regulated in high glucose‐induced human proximal tubular epithelial cells (HK‐2 cells). Moreover, we found that overexpression or knockdown of ARAP1‐AS2 could regulate fibrosis and HK‐2 cell proliferation through EGFR/TGF‐β/Smad3 signalling. RNA pulldown assays revealed that ARAP1‐AS2 directly interacts with ARAP1. Coimmunoprecipitation, dual‐immunofluorescence and ubiquitination assays showed that ARAP1 may maintain persistent EGFR activation by reducing EGFR ubiquitination through competing with Cbl for CIN85 binding. Taken together, our results suggest that the lncRNA ARAP1‐AS2 may promote high glucose‐induced proximal tubular cell injury via persistent EGFR/TGF‐β/Smad3 pathway activation by interacting with ARAP1.

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Section: Discussionmentioning

confidence: 99%

LncRNA ARAP1‐AS2 promotes high glucose‐induced human proximal tubular cell injury via persistent transactivation of the EGFR by interacting with ARAP1

Tian

et al. 2020

J Cellular Molecular Medi

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“…Long noncoding RNA (lncRNA) is one type of noncoding RNA, which is longer than 200nt and without coding potential. 4 LncRNA has been widely studied in various diseases, including diabetes, 5 cardiovascular disease 6 and bone disease. 7 LncRNA can be classified as intronic lncRNA, intergenic lncRNA, promoter associated lncRNA, antisense lncRNA, and untranslated region (UTR) associated lncRNA.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2</p>

Wang

2020

OTT

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Aim: Long noncoding RNA (lncRNA) have proved to be important regulators in various diseases. CDKN2B-AS1 was a newly identified tumor-related lncRNA, and previous studies have reported its function in laryngeal squamous cancer and osteosarcoma. However, the function and mechanism of lncRNA CDKN2B-AS1 in lung cancer are still unknown. Methods: Cell proliferation, invasion, migration and apoptosis were detected via CCK-8, transwell assay and Western blot. Bioinformatics analysis was used to predict the potential target of CDKN2B-AS1. A rescue experiment was performed to identify the relationship between CDKN2B-AS1 and miR-378b. Results: The expression of lncRNA CDKN2B-AS1 was significantly upregulated in lung cancer tissues and cell lines. Overexpression of CDKN2B-AS1 promoted cell proliferation, invasion and reduced cell apoptosis. Knockdown of CDKN2B-AS1 inhibited cell proliferation, invasion and increased cell apoptosis. Bioinformatics analysis predicted that miR-378b was the direct target. We also provided evidence that NR2C2 was the target of miR-378b. The expression of NR2C2 was significantly upregulated in lung cancer tissues and cell lines. The rescue experiment further confirmed the relationship between CDKN2B-AS1 and miR-378b. Overexpression of miR-378b completely reversed the function of CDKN2B-AS1. Conclusion: Taken together, our results comprehensively analyzed the function of CDKN2B-AS1 in lung cancer and provided a possible mechanism that CDKN2B-AS1 facilitates lung cancer development by regulating miR-378b and NR2C2. Thus, our study offers a potential therapeutic target for treating lung cancer.

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“…Several ceRNAs have been shown to interact with TFs, miRNAs, or lncRNAs that result in altered gene expression during disease and cancer progression (Tay et al, 2014). In DN, several studies reported function of lncRNA as ceRNAs in affecting signaling pathways (Chen et al, 2019;Ji et al, 2019). In this study, we identified DEGs as ceRNAs that have negative coexpression with the shared miRNAs, let-7a-5p, miR-21, miR-30a, miR-29b, etc.…”

Section: Discussionmentioning

confidence: 87%

Identification of Cooperative Gene Regulation Among Transcription Factors, LncRNAs, and MicroRNAs in Diabetic Nephropathy Progression

Chen

Wang

et al. 2020

Front. Genet.

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The pathogenesis of diabetic nephropathy (DN) is accompanied by alterations in biological function and signaling pathways regulated through complex molecular mechanisms. A number of regulatory factors, including transcription factors (TFs) and non-coding RNAs (ncRNAs, including lncRNAs and miRNAs), have been implicated in DN; however, it is unclear how the interactions among these regulatory factors contribute to the development of DN pathogenesis. In this study, we developed a network-based analysis to decipher interplays between TFs and ncRNAs regulating progression of DN by combining omics data with regulatory factor-target information. To accomplish this, we identified differential expression programs of mRNAs and miRNAs during early DN (EDN) and established DN. We then uncovered putative interactive connections among miRNA-mRNA, lncRNA-miRNA, and lncRNA-mRNA implicated in transcriptional control. This led to the identification of two lncRNAs (MALAT1 and NEAT1) and the three TFs (NF-κB, NFE2L2, and PPARG) that likely cooperate with a set of miRNAs to modulate EDN and DN target genes. The results highlight how crosstalk among TFs, lncRNAs, and miRNAs regulate the expression of genes both transcriptionally and post-transcriptionally, and our findings provide new insights into the molecular basis and pathogenesis of progressive DN.

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The topological key lncRNA H2k2 from the ceRNA network promotes mesangial cell proliferation in diabetic nephropathyviathe miR‐449a/b/Trim11/Mek signaling pathway

Cited by 32 publications

References 43 publications

LncRNA ARAP1‐AS2 promotes high glucose‐induced human proximal tubular cell injury via persistent transactivation of the EGFR by interacting with ARAP1

LncRNA ARAP1‐AS2 promotes high glucose‐induced human proximal tubular cell injury via persistent transactivation of the EGFR by interacting with ARAP1

<p>Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2</p>

Identification of Cooperative Gene Regulation Among Transcription Factors, LncRNAs, and MicroRNAs in Diabetic Nephropathy Progression

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