Silencing of UCA1 Protects Against MPP+-Induced Cytotoxicity in SK-N-SH Cells via Modulating KCTD20 Expression by Sponging miR-423-5p
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,...
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| Veröffentlicht in: | Neurochemical research 2021-04, Vol.46 (4), p.878-887 |
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| creator | Zheng, Yanhua Liu, Junpeng Zhuang, Jiajun Dong, Xiaoyan Yu, Miao Li, Zhihui |
| description | 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. |
| doi_str_mv | 10.1007/s11064-020-03214-9 |
| format | Article |
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+
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.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-020-03214-9</identifier><identifier>PMID: 33464446</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Bladder cancer ; Cell Biology ; Cell injury ; Cell viability ; Cholecystokinin ; Cytotoxicity ; Flow cytometry ; Immunoprecipitation ; Movement disorders ; MPP ; Neurochemistry ; Neurodegenerative diseases ; Neurology ; Neurosciences ; Original Paper ; Parkinson's disease ; Pathogenesis ; Potassium ; Toxicity ; Urothelial carcinoma</subject><ispartof>Neurochemical research, 2021-04, Vol.46 (4), p.878-887</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-783d45c0e3ae6bcf697dffdbbc7df34cec8b3fa0015b52f18b2ce13a94c230f43</citedby><cites>FETCH-LOGICAL-c375t-783d45c0e3ae6bcf697dffdbbc7df34cec8b3fa0015b52f18b2ce13a94c230f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-020-03214-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-020-03214-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33464446$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Yanhua</creatorcontrib><creatorcontrib>Liu, Junpeng</creatorcontrib><creatorcontrib>Zhuang, Jiajun</creatorcontrib><creatorcontrib>Dong, Xiaoyan</creatorcontrib><creatorcontrib>Yu, Miao</creatorcontrib><creatorcontrib>Li, Zhihui</creatorcontrib><title>Silencing of UCA1 Protects Against MPP+-Induced Cytotoxicity in SK-N-SH Cells via Modulating KCTD20 Expression by Sponging miR-423-5p</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>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.</description><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bladder cancer</subject><subject>Cell Biology</subject><subject>Cell injury</subject><subject>Cell viability</subject><subject>Cholecystokinin</subject><subject>Cytotoxicity</subject><subject>Flow cytometry</subject><subject>Immunoprecipitation</subject><subject>Movement disorders</subject><subject>MPP</subject><subject>Neurochemistry</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Parkinson's disease</subject><subject>Pathogenesis</subject><subject>Potassium</subject><subject>Toxicity</subject><subject>Urothelial carcinoma</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9v1DAQxS0EokvhC3BAlrggIcPY4_w7rkKhVVtYse3ZShxn5SprBztB3Q_A98bbbanEoac5vN97M6NHyFsOnzhA8TlyDrlkIIABCi5Z9YwseFYgyyvA52QBmGTkFRyRVzHeACSb4C_JEaLMpZT5gvxZ28E4bd2G-p5e10tOV8FPRk-RLjeNdXGil6vVR3bmulmbjta7yU_-1mo77ah1dH3OvrP1Ka3NMET62zb00nfz0Ez7yPP66osAenI7BhOj9Y62O7oevdvs1a39yaRAlo2vyYu-GaJ5cz-PyfXXk6v6lF38-HZWLy-YxiKbWFFiJzMNBhuTt7rPq6Lr-65tdZootdFli32T_szaTPS8bIU2HJtKaoHQSzwmHw65Y_C_ZhMntbVRp8sbZ_wclZBFBRI4YkLf_4fe-Dm4dF2iqkoClKVIlDhQOvgYg-nVGOy2CTvFQe1LUoeSVCpJ3ZWkqmR6dx89t1vT_bM8tJIAPAAxSW5jwuPuJ2L_AgZmmrg</recordid><startdate>20210401</startdate><enddate>20210401</enddate><creator>Zheng, Yanhua</creator><creator>Liu, Junpeng</creator><creator>Zhuang, Jiajun</creator><creator>Dong, Xiaoyan</creator><creator>Yu, Miao</creator><creator>Li, Zhihui</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20210401</creationdate><title>Silencing of UCA1 Protects Against MPP+-Induced Cytotoxicity in SK-N-SH Cells via Modulating KCTD20 Expression by Sponging miR-423-5p</title><author>Zheng, Yanhua ; Liu, Junpeng ; Zhuang, Jiajun ; Dong, Xiaoyan ; Yu, Miao ; Li, Zhihui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-783d45c0e3ae6bcf697dffdbbc7df34cec8b3fa0015b52f18b2ce13a94c230f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bladder cancer</topic><topic>Cell Biology</topic><topic>Cell injury</topic><topic>Cell viability</topic><topic>Cholecystokinin</topic><topic>Cytotoxicity</topic><topic>Flow cytometry</topic><topic>Immunoprecipitation</topic><topic>Movement disorders</topic><topic>MPP</topic><topic>Neurochemistry</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Parkinson's disease</topic><topic>Pathogenesis</topic><topic>Potassium</topic><topic>Toxicity</topic><topic>Urothelial carcinoma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Yanhua</creatorcontrib><creatorcontrib>Liu, Junpeng</creatorcontrib><creatorcontrib>Zhuang, Jiajun</creatorcontrib><creatorcontrib>Dong, Xiaoyan</creatorcontrib><creatorcontrib>Yu, Miao</creatorcontrib><creatorcontrib>Li, Zhihui</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Yanhua</au><au>Liu, Junpeng</au><au>Zhuang, Jiajun</au><au>Dong, Xiaoyan</au><au>Yu, Miao</au><au>Li, Zhihui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silencing of UCA1 Protects Against MPP+-Induced Cytotoxicity in SK-N-SH Cells via Modulating KCTD20 Expression by Sponging miR-423-5p</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2021-04-01</date><risdate>2021</risdate><volume>46</volume><issue>4</issue><spage>878</spage><epage>887</epage><pages>878-887</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><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.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33464446</pmid><doi>10.1007/s11064-020-03214-9</doi><tpages>10</tpages></addata></record> |
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| subjects | Apoptosis Biochemistry Biomedical and Life Sciences Biomedicine Bladder cancer Cell Biology Cell injury Cell viability Cholecystokinin Cytotoxicity Flow cytometry Immunoprecipitation Movement disorders MPP Neurochemistry Neurodegenerative diseases Neurology Neurosciences Original Paper Parkinson's disease Pathogenesis Potassium Toxicity Urothelial carcinoma |
| title | Silencing of UCA1 Protects Against MPP+-Induced Cytotoxicity in SK-N-SH Cells via Modulating KCTD20 Expression by Sponging miR-423-5p |
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