Bioinformatics Analysis of Weighted Genes in Diabetic Retinopathy

You, Zhipeng; Zhang, Yulan; Li, Bingyang; Zhu, Xingen; Shi, Ke

doi:10.1167/iovs.18-25515

Cited by 22 publications

(17 citation statements)

References 38 publications

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“…With the rapid development of next-generation sequencing technology and bioinformatics, more and more non-coding RNAs (ncRNAs) are identified to be involved in the human multiple diseases. 17,18 LncRNA PVT1 has been reported as a diabetes-related ncRNA transcript. [19][20][21] In this research, we found that the lncRNA PVT1 was remarkedly up-regulated in the diabetic cataract (DC) tissue and high glucose (HG)-administrated HLE B-3 cells.…”

Section: Discussionmentioning

confidence: 99%

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SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

Yang

Tian

2019

J Cellular Molecular Medi

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Emerging evidence illustrates the critical roles of long non‐coding RNAs (lncRNAs) in the diabetes. However, the deepgoing regulation of lncRNA PVT1 in the diabetic cataract (DC) is still unclear. Here, present research investigates the pathologic roles and underlying mechanism by which lncRNA PVT1 regulates the DC pathogenesis. Human lens epithelial (HLE) B‐3 cells were induced by the high glucose (HG) to simulate the DC microenvironment models. Results revealed that lncRNA PVT1 expression was up‐regulated in the HG‐induced HLE B‐3 cells as compared to the normal glucose group. Transcription factor SP1 could bind with the promoter region of PVT1 and activate its transcription. Functionally, PVT1 knock‐down could repress the proliferation and promote the apoptosis of HLE B‐3 cells. Mechanistically, PVT1 acted as the ‘miRNA sponge’ to target miR‐214‐3p/MMP2 axis. This finding revealed a novel insight of lncRNA PVT1 for the DC pathogenesis, providing an inspiration for the DC mechanism.

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Section: Discussionmentioning

confidence: 99%

“…With the rapid development of next‐generation sequencing technology and bioinformatics, more and more non‐coding RNAs (ncRNAs) are identified to be involved in the human multiple diseases . LncRNA PVT1 has been reported as a diabetes‐related ncRNA transcript .…”

Section: Discussionmentioning

confidence: 99%

SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

Yang

Tian

2019

J Cellular Molecular Medi

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“…Bioinformatic analysis is a well-established method that is widely used to help researchers identify potential biomarkers. 27 Thus, we performed bioinformatic analysis of the GEO database to reveal that TRIM59 was one of the most upregulated genes in retinoblastoma samples, which was consistent among the three datasets analyzed. Through qRT-PCR and immunoblotting, we verified that the level of TRIM59 in retinoblastoma cells differed significantly from that in control cells.…”

Section: Discussionmentioning

confidence: 76%

TRIM59 Promotes Retinoblastoma Progression by Activating the p38–MAPK Signaling Pathway

Shang

You

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Retinoblastoma is a malignant tumor of the developing retina that mostly occurs in children. Our study aimed to investigate the effect of tripartite motif-containing protein 59 (TRIM59) on retinoblastoma growth and the underlying mechanisms. METHODS. We performed bioinformatic analysis of three datasets (GSE24673, GSE97508, and GSE110811) from the Gene Expression Omnibus database. Quantitative reversetranscription PCR and immunoblotting of three retinoblastoma cell lines were conducted to verify TRIM59 as a differentially expressed gene. Specific siRNAs were used to inhibit TRIM59 expression in the HXO-Rb44 cell line. A lentiviral vector was transfected into the Y79 cell line to overexpress TRIM59. The effects of TRIM59 on retinoblastoma cell proliferation, cell cycling, and apoptosis were explored in vitro using the abovementioned cell lines. The effect of TRIM59 expression on retinoblastoma cell proliferation was evaluated in a mouse xenograft tumor model. RESULTS. TRIM59 expression in three retinoblastoma cell lines was remarkably elevated compared with normal control. Knocking down TRIM59 expression remarkably suppressed cell proliferation and growth and promoted cell apoptosis in HXO-Rb44 cells, whereas TRIM59 overexpression promoted tumor progression in Y79 cells. Silencing TRIM59 also markedly inhibited in vivo tumor growth in the xenograft model. Mechanistic studies revealed that TRIM59 upregulated phosphorylated p38, p-JNK1/2, p-ERK1/2, and p-c-JUN expression in retinoblastoma cells. Notably, the p38 inhibitor SB203580 attenuated the effects of TRIM59 on cell proliferation, apoptosis, and the G 1 /S phase transition. CONCLUSIONS. TRIM59 plays an oncogenic role in retinoblastoma and exerts its tumorpromotive function by activating the p38-mitogen-activated protein kinase pathway.

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“…It is well known that the initiation and progression of diabetesinduced multisystem complications are complex pathological processes associated with inflammation (23,30,43,59). Pyroptosis is a novel type of programmed cell death related to the activation of inflammation (4).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA KCNQ1OT1 induces pyroptosis in diabetic corneal endothelial keratopathy

Zhang

Song

et al. 2020

American Journal of Physiology-Cell Physiology

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Diabetic corneal endothelial keratopathy is an intractable ocular complication characterized by corneal edema and endothelial decompensation, which seriously threaten vision. It has been suggested that diabetes is associated with pyroptosis, a type of programmed cell death via the activation of inflammation. Long noncoding RNA KCNQ1OT1 is commonly associated with various pathophysiological mechanisms of diabetic complications, including diabetic cardiomyopathy and diabetic retinopathy. However, whether KCNQ1OT1 is capable of regulating pyroptosis and participates in the pathogenesis of diabetic corneal endothelial keratopathy remains unknown. The aim of this study was to investigate the mechanisms of KCNQ1OT1 in diabetic corneal endothelial keratopathy. Here, we reveal that KCNQ1OT1 and pyroptosis can be triggered in diabetic human and rat corneal endothelium, along with the high glucose-treated corneal endothelial cells. However, miR-214 expression was substantially decreased in vivo and in experiments with cultured cells. LDH assay was also used to verify the existence of pyroptosis in high glucose-treated cells. Bioinformatics prediction and luciferase assays showed that KCNQ1OT1 may function as a competing endogenous RNA binding miR-214 to regulate the expression of caspase-1. To further analyze the KCNQ1OT1-mediated mechanism, miR-214 mimic and inhibitor were introduced into the high glucose-treated corneal endothelial cells. The results showed that upregulation of miR-214 attenuated pyroptosis; conversely, knockdown of miR-214 promoted it. In addition, KCNQ1OT1 knockdown by a small interfering RNA decreased pyroptosis factors expressions but enhanced miR-214 expression in corneal endothelial cells. To understand the signaling mechanisms underlying the prepyroptotic properties of KCNQ1OT1, si-KCNQ1OT1 was cotransfected with or without miR-214 inhibitor. The results showed that pyroptosis was repressed after silencing KCNQ1OT1 but was reversed by cotransfection with miR-214 inhibitor, suggesting that KCNQ1OT1 mediated pyroptosis induced by high glucose via targeting miR-214. Therefore, the KCNQ1OT1/miR-214/caspase-1 signaling pathway represents a new mechanism of diabetic corneal endothelial keratopathy progression, and KCNQ1OT1 could potentially be a novel therapeutic target.

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Bioinformatics Analysis of Weighted Genes in Diabetic Retinopathy

Cited by 22 publications

References 38 publications

SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

TRIM59 Promotes Retinoblastoma Progression by Activating the p38–MAPK Signaling Pathway

Long noncoding RNA KCNQ1OT1 induces pyroptosis in diabetic corneal endothelial keratopathy

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