MicroRNA‑198 contributes to lupus nephritis progression by inhibition of phosphatase and tensin homology deleted on chromosome ten expression

Cui,Danyu; Zhu,Dingji; Ren,Hao; Lin,Jingli; Lai,Weinan; Huang,Qin; Zhao,Jinjun; Yang,Min

doi:10.3892/mmr.2017.7527

MicroRNA‑198 contributes to lupus nephritis progression by inhibition of phosphatase and tensin homology deleted on chromosome ten expression

Authors:
- Danyu Cui
- Dingji Zhu
- Hao Ren
- Jingli Lin
- Weinan Lai
- Qin Huang
- Jinjun Zhao
- Min Yang
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Affiliations: Department of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
Published online on: September 19, 2017 https://doi.org/10.3892/mmr.2017.7527
Pages: 7813-7820

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Abstract

A number of short noncoding microRNAs (miRs) have been demonstrated to be highly expressed in many kidney diseases such as renal cancer and lupus nephritis (LN); however, these results have not been extensively investigated. The aim of the present study was to investigate the expression and function of miR‑198 in LN based on the previous studies. miR‑198 expression level in systemic lupus erythematosus (SLE) patients was determined to determine its clinicopathological significance and effect on glomerular cell proliferation. It was demonstrated that higher expression of miR‑198 was observed in patients with SLE, and was correlated with disease activity. Bioinformatics prediction and luciferase assays were used to demonstrate that miR‑198 could directly bind to the phosphatase and tensin homology deleted on chromosome ten (PTEN) 3'‑untranslated region. Furthermore, miR‑198 overexpression reduced PTEN expression levels, while miR‑198 silencing increased its expression at both the mRNA and protein level. Furthermore, there was a negative association between miR‑198 and PTEN in the patients with active SLE. Thus, miR‑198 may promote proliferation and contribute to SLE progression by targeting PTEN.

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