We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Silencing of UCA1 Protects Against MPP+-Induced Cytotoxicity in SK-N-SH Cells via Modulating KCTD20 Expression by Sponging miR-423-5p.
- Authors
Zheng, Yanhua; Liu, Junpeng; Zhuang, Jiajun; Dong, Xiaoyan; Yu, Miao; Li, Zhihui
- Abstract
Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder. Long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been implicated in PD development. Nevertheless, little insight has been gained on the mechanisms of UCA1 in PD pathogenesis. The levels of UCA1, miR-423-5p and potassium channel tetramerization domain containing 20 (KCTD20) were assessed by qRT-PCR and western blot. Cell viability was gauged by the CCK-8 assay, and cell apoptosis was detected by flow cytometry. Targeted relationships among UCA1, miR-423-5p and KCTD20 were verified by dual-luciferase reporter and RNA immunoprecipitation assays. Our data showed that MPP+ induced UCA1 expression in SK-N-SH cells. UCA1 silencing protected against MPP+-evoked cytotoxicity in SK-N-SH cells. UCA1 functioned as a miR-423-5p sponge, and the protective impact of UCA1 silencing on MPP+-evoked cytotoxicity was mediated by miR-423-5p. KCTD20 was a direct target of miR-423-5p, and miR-423-5p overexpression mitigated MPP+-triggered cell injury by down-regulating KCTD20. Furthermore, UCA1 regulated KCTD20 expression by acting as a sponge of miR-423-5p in SK-N-SH cells. Our study first identified that the silencing of UCA1 protected SK-N-SH cells from MPP+-evoked cytotoxicity at least in part by targeting the miR-423-5p/KCTD20 axis.
- Subjects
CIRCULAR RNA; LINCRNA; PARKINSON'S disease; NEURODEGENERATION; FLOW cytometry; CELL survival
- Publication
Neurochemical Research, 2021, Vol 46, Issue 4, p878
- ISSN
0364-3190
- Publication type
Article
- DOI
10.1007/s11064-020-03214-9