Deduction of Novel Genes Potentially Involved in Upper Tract Urothelial Carcinoma Using Next-Generation Sequencing and Bioinformatics Approaches

Lee, Hsiang Ying; Chen, Yi-Jen; Li, Ching Chia; Li, Wei Ming; Hsu, Ya Ling; Yeh, Hsin Chih; Ke, Hung‐Lung; Huang, Ching‐Wen; Li, Chien‐Feng; Wu, Wen‐Jeng; Kuo, Po Lin

doi:10.7150/ijms.29560

Cited by 8 publications

(5 citation statements)

References 70 publications

(65 reference statements)

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“…Differentially expressed miRNAs greater than 2.0‐fold changes between young and senescent cell groups were indicated with reads per million (RPM) > 10 (Figure 1A). 20 …”

Section: Methodsmentioning

confidence: 99%

Hsa‐miR‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

Lee

et al. 2023

J Cellular Molecular Medi

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We explored the roles of hsa‐microRNA (miR)‐409‐3p in senescence and signalling mechanism of human endothelial progenitor cells (EPCs). Hsa‐miR‐409‐3p was found upregulated in senescent EPCs. Overexpression of miRNA mimics in young EPCs inhibited angiogenesis. In senescent EPCs, compared to young EPCs, protein phosphatase 2A (PP2A) was downregulated, with activation of p38/JNK by phosphorylation. Young EPCs treated with siPP2A caused inhibited angiogenesis with activation of p38/JNK, similar to findings in senescent EPCs. Time series analysis showed, in young EPCs treated with hsa‐miR‐409‐3p mimics, PP2A was steadily downregulated for 72 h, while p38/JNK was activated with a peak at 48 hours. The inhibited angiogenesis of young EPCs after miRNA‐409‐3p mimics treatment was reversed by the p38 inhibitor. The effect of hsa‐miR‐409‐3p on PP2A signalling was attenuated by exogenous VEGF. Analysis of human peripheral blood mononuclear cells (PBMCs) obtained from healthy people revealed hsa‐miR‐409‐3p expression was higher in those older than 65 years, compared to those younger than 30 years, regardless of gender. In summary, hsa‐miR‐409‐3p was upregulated in senescent EPCs and acted as a negative modulator of angiogenesis via targeting protein phosphatase 2 catalytic subunit alpha (PPP2CA) gene and regulating PP2A/p38 signalling. Data from human PBMCs suggested hsa‐miR‐409‐3p a potential biomarker for human ageing.

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“…Differentially expressed miRNAs greater than 2.0‐fold changes between young and senescent cell groups were indicated with reads per million (RPM) > 10 (Figure 1A). 20 …”

Section: Methodsmentioning

confidence: 99%

Hsa‐miR‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

Lee

et al. 2023

J Cellular Molecular Medi

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“…Only select transcripts and pathways, such as hepatocyte growth factor and tumor necrosis factor (TNF) signaling or genes involved in adhesion, were differentially dysregulated between the two [36][37][38], but with a clear separation from renal cell carcinoma [39]. In a small study comparing healthy urothelial tissue and UTUC expression profiles, the authors mainly reported differences in the cell cycle and extracellular matrix-regulated genes [40].…”

Section: Rna Expression Profiles Of Utucmentioning

confidence: 99%

Molecular Characterization of Upper Tract Urothelial Carcinoma in the Era of Next-generation Sequencing: A Systematic Review of the Current Literature

et al. 2020

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“…The difference of miRNA expression level between two groups more than twofolds were considered as significance (Figure 1C ). 25 , 30 …”

Section: Methodsmentioning

confidence: 99%

Hsa‐miR‐134‐5p predicts cardiovascular risk in circulating mononuclear cells and improves angiogenic action of senescent endothelial progenitor cells

Tien,

Wu,

Chang

et al. 2024

J Cellular Molecular Medi

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This research explores the role of microRNA in senescence of human endothelial progenitor cells (EPCs) induced by replication. Hsa‐miR‐134‐5p was found up‐regulated in senescent EPCs where overexpression improved angiogenic activity. Hsa‐miR‐134‐5p, which targeted transforming growth factor β‐activated kinase 1‐binding protein 1 (TAB1) gene, down‐regulated TAB1 protein, and inhibited phosphorylation of p38 mitogen‐activated protein kinase (p38) in hsa‐miR‐134‐5p‐overexpressed senescent EPCs. Treatment with siRNA specific to TAB1 (TAB1si) down‐regulated TAB1 protein and subsequently inhibited p38 activation in senescent EPCs. Treatment with TAB1si and p38 inhibitor, respectively, showed angiogenic improvement. In parallel, transforming growth factor Beta 1 (TGF‐β1) was down‐regulated in hsa‐miR‐134‐5p‐overexpressed senescent EPCs and addition of TGF‐β1 suppressed the angiogenic improvement. Analysis of peripheral blood mononuclear cells (PBMCs) disclosed expression levels of hsa‐miR‐134‐5p altered in adult life, reaching a peak before 65 years, and then falling in advanced age. Calculation of the Framingham risk score showed the score inversely correlates with the hsa‐miR‐134‐5p expression level. In summary, hsa‐miR‐134‐5p is involved in the regulation of senescence‐related change of angiogenic activity via TAB1‐p38 signalling and via TGF‐β1 reduction. Hsa‐miR‐134‐5p has a potential cellular rejuvenation effect in human senescent EPCs. Detection of human PBMC‐derived hsa‐miR‐134‐5p predicts cardiovascular risk.

show abstract

Deduction of Novel Genes Potentially Involved in Upper Tract Urothelial Carcinoma Using Next-Generation Sequencing and Bioinformatics Approaches

Cited by 8 publications

References 70 publications

Hsa‐miR‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

Hsa‐miR‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

Molecular Characterization of Upper Tract Urothelial Carcinoma in the Era of Next-generation Sequencing: A Systematic Review of the Current Literature

Hsa‐miR‐134‐5p predicts cardiovascular risk in circulating mononuclear cells and improves angiogenic action of senescent endothelial progenitor cells

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