Long non-coding RNA Rpph1 promotes inflammation and proliferation of mesangial cells in diabetic nephropathy via an interaction with Gal-3

Zhang, Pan-Yang; Sun, Yan; Peng, Rui; Chen, Wenyun; Fu, Xiafei; Zhang, Luyu; Peng, Huimin; Zhang, Zheng

doi:10.1038/s41419-019-1765-0

Cited by 74 publications

(66 citation statements)

References 59 publications

(57 reference statements)

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“…Rpph1 was shown to bind Gal-3, a biomarker of diabetic nephropathy, which itself was increased in diseased renal tissue and enhanced mesangial cells proliferation. Further experiments suggested that Rpph1 somehow enhances the expression of Gal-3, which itself was shown to play a role in the regulation of inflammation and proliferation of mesangial cells via the Mek/ Erk pathway (Zhang et al 2019).…”

Section: Rpph1mentioning

confidence: 99%

RNA polymerase III transcription as a disease factor

Yeganeh

Hernandez

2020

Genes Dev.

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RNA polymerase (Pol) III is responsible for transcription of different noncoding genes in eukaryotic cells, whose RNA products have well-defined functions in translation and other biological processes for some, and functions that remain to be defined for others. For all of them, however, new functions are being described. For example, Pol III products have been reported to regulate certain proteins such as protein kinase R (PKR) by direct association, to constitute the source of very short RNAs with regulatory roles in gene expression, or to control microRNA levels by sequestration. Consistent with these many functions, deregulation of Pol III transcribed genes is associated with a large variety of human disorders. Here we review different human diseases that have been linked to defects in the Pol III transcription apparatus or to Pol III products imbalance and discuss the possible underlying mechanisms.

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Section: Rpph1mentioning

confidence: 99%

RNA polymerase III transcription as a disease factor

Yeganeh

Hernandez

2020

Genes Dev.

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“…Studies have also begun to demonstrate the participation and regulatory mechanism of non-coding rnas (ncrnas) on dn development (6,7). circular rnas (circrnas) are a novel class of endogenous ncrnas, which mediate diverse physiological and pathological changes in the human body (8), including dn, and are characterized by a covalently-closed loop formed by back-splicing between the 5' to 3' ends of the polya tail (9,10).…”

Section: Introductionmentioning

confidence: 99%

A novel identified circular RNA, circ_0000491, aggravates the extracellular matrix of diabetic nephropathy glomerular mesangial cells through suppressing miR‑101b by targeting TGFβRI

Mou¹,

Chenv²,

Zhou³

et al. 2020

Mol Med Rep

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circular rnas (circrnas) have crucial roles in various diseases; however, the mechanisms of action underlying circrnas in the occurrence and development of diabetic nephropathy (dn) remains largely unknown. The present study investigated the differentially expressed circrnas in the dn mice kidney cortex using circrna sequencing and elucidated the role of circrnas in mesangial cells. it was revealed that 40 circrnas were unconventionally expressed, including 18 upregulated circrnas and 22 downregulated circRNAs. Furthermore, circ_0000491 levels were significantly augmented in both dn mice and high glucose (HG, 30 mM)-induced mouse mesangial cells (MeS13 cells). Knockdown of circ_0000491 significantly suppressed the increase of vimentin, fibronectin and α-smooth muscle actin, as well as collagen type i, iii and iV, whilst reversing the decrease of e-cadherin in HG-induced MeS13 cells. it was further revealed that circrna_0000491 sponged mir-101b and that mir-101b directly targets TGFβri. in addition, the expression levels of mir-101b were negatively associated with the transcriptional level of circrna_0000491 and mir-101b inhibitors reversed the suppression of extracellular matrix (ecM)-associated protein synthesis mediated by knocking-down circrna_0000491. in conclusion, the present study investigated the circrna_0000491/mir-101b/TGFβri axis in ecM accumulation and fibrosis-associated protein expression levels of mesangial cells, which suggested that circRNA_0000491 may be beneficial for the development of an effective therapeutic target for dn.

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“…RPPH1 is also thought to be involved in the inflammatory pathogenesis of diabetic nephropathy. Indeed, in a mouse model of diabetic nephropathy, RPPH1 was abnormally overexpressed in renal tissue and enhanced the release of inflammatory cytokines, including tumor necrosis factor-α and monocyte chemotactic protein-1 (9). Moreover, Zhang et al (10) demonstrated that RPPH1 upregulation enhanced the proliferative and colony formation abilities of breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

lncRNA RPPH1 promotes non‑small cell lung cancer progression through the miR‑326/WNT2B axis

Cheng

Liang

et al. 2020

Oncol Lett

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Long non-coding RNAs (lncRNAs) serve important regulatory roles in human tumors. The aim of the present study was to examine the role of ribonuclease P RNA component H1 (RPPH1) in non-small cell lung cancer (NSCLC). RPPH1 expression was assessed in datasets from The Cancer Genome Atlas, as well as lung cancer cell lines and patients with NSCLC. RPPH1 was significantly upregulated in NSCLC cell lines, compared with a normal lung epithelial cell line. Moreover, high RPPH1 expression was associated with poor overall survival and disease progression. RPPH1 was knocked down in A549 and H1299 cells using short hairpin (sh) RNA constructs, and the expressions of target genes and proteins were determined by reverse transcription-quantitative PCR and western blotting. Cell invasion potential was also determined using Transwell Matrigel assays. Compared with the negative control, RPPH1 silencing significantly reduced the number of invading cells, increased E-cadherin expression and reduced vimentin protein expression. Cell resistance to cisplatin/cis-diamminedichloridoplatinum (CDDP) was also evaluated using Cell Counting Kit-8 and colony formation assays. RPPH1 overexpression increased the resistance of A549 and H1299 cells to CDDP. Moreover, the potential interactions between RPPH1, microRNA (miR)-326 and Wnt family member 2B (WNT2B) were investigated using luciferase reporter assays and co-transfection experiments. MiR-326 expression was directly inhibited by RPPH1. In A549 cells co-transfected with shRPPH1 and miR-326 inhibitor, the invading cell number significantly increased compared with cells transfected with shRPPH1 alone. In addition, E-cadherin expression levels were reduced, and vimentin was upregulated. MiR-326 overexpression partially reduced the resistance of A549 cells to CDDP induced by RPPH1 overexpression. WNT2B expression was directly suppressed using miR-326. A549 cells co-transfected with a miR-326 mimic and a WNT2B overexpression vector demonstrated increased invasion potential, reduced E-cadherin and increased vimentin protein expression levels, compared with cells transfected with the mimic alone. miR-326 overexpression reduced CDDP resistance in A549 cells. However, co-transfection with WNT2B partially enhanced CDDP resistance, compared with the mimic alone. In conclusion, RPPH1 promoted NSCLC progression and lung cancer cell resistance to CDDP through miR-326 and WNT2B.

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Long non-coding RNA Rpph1 promotes inflammation and proliferation of mesangial cells in diabetic nephropathy via an interaction with Gal-3

Cited by 74 publications

References 59 publications

RNA polymerase III transcription as a disease factor

RNA polymerase III transcription as a disease factor

A novel identified circular RNA, circ_0000491, aggravates the extracellular matrix of diabetic nephropathy glomerular mesangial cells through suppressing miR‑101b by targeting TGFβRI

lncRNA RPPH1 promotes non‑small cell lung cancer progression through the miR‑326/WNT2B axis

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