期刊
NEUROCHEMICAL RESEARCH
卷 46, 期 4, 页码 878-887出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-020-03214-9
关键词
Parkinson's disease (PD); UCA1; miR-423-5p; KCTD20; Cytotoxicity
This study demonstrated that UCA1 plays a role in Parkinson's disease pathogenesis by modulating the miR-423-5p/KCTD20 axis, thus protecting SK-N-SH cells from MPP+-evoked cytotoxicity.
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.
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