Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells

The aim of this study was to explore whether the long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1)/miR-34a/Snail1 and NEAT1/miR-204/Zeb1 pathways are involved in epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Primary human LECs (HLECs) were separated and cultured. Our results identified that TGF-β2 induces NEAT1 overexpression in a dose-dependent manner and a time-dependent manner. Additionally, TGF-β2 induced downregulation of E-cadherin and upregulation of fibronectin in primary HLECs through a NEAT1-dependent mechanism. Microarray analysis showed that NEAT1 overexpression inhibited the miR-34a and miR-204 levels in the LECs. The expression of miR-34a and miR-204 was decreased, and the levels of Snail1 and Zeb1 were elevated in human posterior capsule opacification- (PCO-) attached LECs and the LECs obtained from anterior subcapsular cataract (ASC) by quantitative RT-PCR (qRT-PCR). Mechanistic studies revealed that NEAT1 negatively regulates miR-34a or miR-204, and miR-34a or miR-204 directly targets Snail1 or Zeb1 by luciferase assay and RNA-binding protein immunoprecipitation assay, respectively. Overall, the NEAT1/miR-34a/Snail1 and NEAT1/miR-204/Zeb1 pathways are involved in TGF-β2-induced EMT of HLECs. In summary, TGF-β2 induces NEAT1 overexpression, which in turn suggests that NEAT1 acts as a ceRNA targeting Snail1 or Zeb1 by binding miR-34a or miR-204, and promotes the progression of EMT of LECs.

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Long Noncoding RNA MALAT1 Acts as a Competing Endogenous RNA to Regulate TGF-β2 Induced Epithelial-Mesenchymal Transition of Lens Epithelial Cells by a MicroRNA-26a-Dependent Mechanism

BioMed Research International ◽

10.1155/2019/1569638 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11

Author(s):

Ning Dong

Keyword(s):

Epithelial Cells ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Rna Binding ◽

Epithelial Mesenchymal Transition ◽

Luciferase Reporter ◽

Lens Epithelial Cells ◽

Mesenchymal Transition ◽

Reporter Assays ◽

Dependent Mechanism

The aim of the present study was to characterize whether the long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/miR-26a/Smad4 axis is involved in epithelial–mesenchymal transition (EMT) of lens epithelial cells (LECs). Primary human LECs were separated and cultured. Microarray analysis showed that a total of 568 lncRNAs are differentially expressed in primary HLECs in the presence of TGF-β2 and MALAT1 is mostly significantly dysregulated lncRNAs, which is increased by nearly 17-fold. In addition, upregulation of MALAT1 and downregulation of miR-26a were detected in human posterior capsule opacification (PCO) attached LECs and the LECs obtained from patients with anterior polar cataracts by quantitative RT-PCR (qRT-PCR). Next, our results showed that TGF-β2 induces overexpression of EMT markers in primary HLECs via a MALAT1-dependent mechanism. The mechanism is that MALAT1 negatively regulates miR-26a and miR-26a directly targets Smad4 by luciferase reporter assays and RNA-binding protein immunoprecipitation assay. In summary, TGF-β2 induces MALAT1 overexpression, which in turn MALAT1 acts as a ceRNA targeting Smad4 by binding miR-26a and promotes the progression of EMT of LECs.

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Knockdown of the Long Noncoding RNA LUCAT1 Inhibits High-Glucose-Induced Epithelial-Mesenchymal Transition through the miR-199a-5p–ZEB1 Axis in Human Renal Tubular Epithelial Cells

BioMed Research International ◽

10.1155/2020/8895003 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

Li-Cai Zhang ◽

Zong-Bin Wei ◽

Shui-Fu Tang

Keyword(s):

Epithelial Cells ◽

High Glucose ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Epithelial Mesenchymal Transition ◽

Negative Control ◽

Tubular Epithelial Cells ◽

Renal Tubular Epithelial Cells ◽

Mesenchymal Transition ◽

Renal Tubular

Renal fibrosis, the leading cause of end-stage renal disease and in which epithelial-mesenchymal transition (EMT) plays a central role, has a complex pathogenesis that is not fully understood. Therefore, we investigated the role of the long noncoding RNA LUCAT1 in the EMT of renal tubular epithelial cells under high-glucose (HG) conditions and the underlying mechanism involved. In this study, we established HG and normal glucose groups of HK-2 cells by treating HK-2 cells 30.0 or 5.5 mmol/L glucose, respectively. To investigate the roles of LUCAT1 and miR-199a-5p in HG-induced EMT, we transfected the HG group with negative control small interfering RNA (siRNA), siRNA targeting LUCAT1, negative control microRNA, or an miR-199a-5p mimic. The results of the quantitative reverse transcription PCR indicated that the LUCAT1 level in the HG group was increased, whereas the miR-199a-5p level was decreased. The EMT in the cells was induced by treatment with HG but was weakened by LUCAT1 knockdown or miR-199a-5p overexpression, which both also inhibited the HG-induced phosphorylation of SMAD3. Moreover, LUCAT1 and ZEB1 mRNA comprised the same microRNA response elements of miR-199a-5p. LUCAT1 knockdown had no effect on the miR-199a-5p level but decreased the HG-induced upregulation of ZEB1. In conclusion, HG conditions induced the upregulation of LUCAT1, and LUCAT1 knockdown inhibited the EMT in HG-treated HK-2 cells. LUCAT1 likely promotes HG-induced EMT through ZEB1 by sponging miR-199a-5p.

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MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines

Journal of Biological Chemistry ◽

10.1074/jbc.m116.750950 ◽

2016 ◽

Vol 292 (1) ◽

pp. 82-99 ◽

Cited By ~ 94

Author(s):

Minoru Terashima ◽

Shoichiro Tange ◽

Akihiko Ishimura ◽

Takeshi Suzuki

Keyword(s):

Lung Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Epigenetic Regulation ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Epithelial Mesenchymal Transition ◽

Cancer Cell Lines ◽

Lung Cancer Cell ◽

Mesenchymal Transition

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Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer

Cell Death and Disease ◽

10.1038/s41419-018-1210-9 ◽

2018 ◽

Vol 9 (12) ◽

Cited By ~ 24

Author(s):

Rong-Hui Li ◽

Min Chen ◽

Jing Liu ◽

Chang-Chun Shao ◽

Cui-Ping Guo ◽

...

Keyword(s):

Breast Cancer ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Poor Prognosis ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition

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An epithelial–mesenchymal transition-related long noncoding RNA signature correlates with the prognosis and progression in patients with bladder cancer

Bioscience Reports ◽

10.1042/bsr20203944 ◽

2021 ◽

Vol 41 (1) ◽

Author(s):

Hang Tong ◽

Tinghao Li ◽

Shun Gao ◽

Hubin Yin ◽

Honghao Cao ◽

...

Keyword(s):

Bladder Cancer ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Epithelial Mesenchymal Transition ◽

Enrichment Analysis ◽

Functional Enrichment Analysis ◽

Risk Groups ◽

Functional Enrichment ◽

Diagnostic Efficacy ◽

Mesenchymal Transition

Abstract Bladder cancer is a common malignant tumour worldwide. Epithelial–mesenchymal transition (EMT)-related biomarkers can be used for early diagnosis and prognosis of cancer patients. To explore, accurate prediction models are essential to the diagnosis and treatment for bladder cancer. In the present study, an EMT-related long noncoding RNA (lncRNA) model was developed to predict the prognosis of patients with bladder cancer. Firstly, the EMT-related lncRNAs were identified by Pearson correlation analysis, and a prognostic EMT-related lncRNA signature was constructed through univariate and multivariate Cox regression analyses. Then, the diagnostic efficacy and the clinically predictive capacity of the signature were assessed. Finally, Gene set enrichment analysis (GSEA) and functional enrichment analysis were carried out with bioinformatics. An EMT-related lncRNA signature consisting of TTC28-AS1, LINC02446, AL662844.4, AC105942.1, AL049840.3, SNHG26, USP30-AS1, PSMB8-AS1, AL031775.1, AC073534.1, U62317.2, C5orf56, AJ271736.1, and AL139385.1 was constructed. The diagnostic efficacy of the signature was evaluated by the time-dependent receiver-operating characteristic (ROC) curves, in which all the values of the area under the ROC (AUC) were more than 0.73. A nomogram established by integrating clinical variables and the risk score confirmed that the signature had a good clinically predict capacity. GSEA analysis revealed that some cancer-related and EMT-related pathways were enriched in high-risk groups, while immune-related pathways were enriched in low-risk groups. Functional enrichment analysis showed that EMT was associated with abundant GO terms or signaling pathways. In short, our research showed that the 14 EMT-related lncRNA signature may predict the prognosis and progression of patients with bladder cancer.

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