Downregulation of lncRNA PVT1 expression inhibits proliferation and migration by regulating p38 expression in prostate cancer
Long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) has been reported to be overexpressed in prostate cancer cells and associated with tumorigenesis in various types of cancer. However, the biological function of lncRNA PVT1 remains largely unknown. The aim of the present study...
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Veröffentlicht in: | Oncology letters 2018-10, Vol.16 (4), p.5160-5166 |
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description | Long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) has been reported to be overexpressed in prostate cancer cells and associated with tumorigenesis in various types of cancer. However, the biological function of lncRNA PVT1 remains largely unknown. The aim of the present study was to investigate the effect of lncRNA PVT1 expression on the proliferation and migration of prostate cancer cells. Stably transfected prostate cancer cells with downregulated expression of lncRNA PVT1 were constructed by an efficient siRNA fragment, followed by confirmation by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Proliferation was assessed using CCK-8, colony formation and xenograft assays, and cell migration was evaluated using a wound healing assay. The PathScan
Intracellular Signaling Array kit was utilized to explore the underlying molecular mechanisms of lncRNA PVT1 expression in prostate cancer cells. RT-qPCR results confirmed that the lncRNA PVT1 expression level was successfully knocked down in prostate cancer cells. When lncRNA PVT1 expression was downregulated in prostate cancer cells, proliferation and migration were significantly inhibited, compared with the control lncRNA PVT1 group. Furthermore, PVT1 knockdown decreased the phosphorylation of p38 in DU145 cells. Therefore, the present study demonstrated that lncRNA PVT1 downregulation inhibits the proliferation and migration of prostate cancer cells, and is associated with p38 phosphorylation. |
doi_str_mv | 10.3892/ol.2018.9305 |
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Intracellular Signaling Array kit was utilized to explore the underlying molecular mechanisms of lncRNA PVT1 expression in prostate cancer cells. RT-qPCR results confirmed that the lncRNA PVT1 expression level was successfully knocked down in prostate cancer cells. When lncRNA PVT1 expression was downregulated in prostate cancer cells, proliferation and migration were significantly inhibited, compared with the control lncRNA PVT1 group. Furthermore, PVT1 knockdown decreased the phosphorylation of p38 in DU145 cells. Therefore, the present study demonstrated that lncRNA PVT1 downregulation inhibits the proliferation and migration of prostate cancer cells, and is associated with p38 phosphorylation.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2018.9305</identifier><identifier>PMID: 30250582</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Androgens ; Care and treatment ; Cell cycle ; Cell growth ; Cervical cancer ; Development and progression ; Genetic aspects ; Genetic regulation ; Health aspects ; Medical research ; Oncogenes ; Oncology ; Ovarian cancer ; Phosphorylation ; Prostate cancer ; Studies ; Wound healing</subject><ispartof>Oncology letters, 2018-10, Vol.16 (4), p.5160-5166</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Wan et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-11d4dd459b3fbd4066a3351461a67aa24597182b4adf4a228d722f9613ac88343</citedby><cites>FETCH-LOGICAL-c471t-11d4dd459b3fbd4066a3351461a67aa24597182b4adf4a228d722f9613ac88343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144883/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144883/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30250582$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wan, Bo</creatorcontrib><creatorcontrib>Wu, Hua-Yan</creatorcontrib><creatorcontrib>Lv, Dao-Jun</creatorcontrib><creatorcontrib>Zhou, Xu-Min</creatorcontrib><creatorcontrib>Zhong, Li-Ren</creatorcontrib><creatorcontrib>Lei, Bin</creatorcontrib><creatorcontrib>Zhang, Shou-Bo</creatorcontrib><creatorcontrib>Mao, Xiang-Ming</creatorcontrib><title>Downregulation of lncRNA PVT1 expression inhibits proliferation and migration by regulating p38 expression in prostate cancer</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>Long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) has been reported to be overexpressed in prostate cancer cells and associated with tumorigenesis in various types of cancer. However, the biological function of lncRNA PVT1 remains largely unknown. The aim of the present study was to investigate the effect of lncRNA PVT1 expression on the proliferation and migration of prostate cancer cells. Stably transfected prostate cancer cells with downregulated expression of lncRNA PVT1 were constructed by an efficient siRNA fragment, followed by confirmation by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Proliferation was assessed using CCK-8, colony formation and xenograft assays, and cell migration was evaluated using a wound healing assay. The PathScan
Intracellular Signaling Array kit was utilized to explore the underlying molecular mechanisms of lncRNA PVT1 expression in prostate cancer cells. RT-qPCR results confirmed that the lncRNA PVT1 expression level was successfully knocked down in prostate cancer cells. When lncRNA PVT1 expression was downregulated in prostate cancer cells, proliferation and migration were significantly inhibited, compared with the control lncRNA PVT1 group. Furthermore, PVT1 knockdown decreased the phosphorylation of p38 in DU145 cells. Therefore, the present study demonstrated that lncRNA PVT1 downregulation inhibits the proliferation and migration of prostate cancer cells, and is associated with p38 phosphorylation.</description><subject>Androgens</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cervical cancer</subject><subject>Development and progression</subject><subject>Genetic aspects</subject><subject>Genetic regulation</subject><subject>Health aspects</subject><subject>Medical research</subject><subject>Oncogenes</subject><subject>Oncology</subject><subject>Ovarian cancer</subject><subject>Phosphorylation</subject><subject>Prostate cancer</subject><subject>Studies</subject><subject>Wound healing</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpdks1v1DAQxSNERau2N84oEhLiwC4ef8TOBWlVvipVgFDhajmJk3XltVM7AXrgf8fWbrddfLGt95s3mtEriueAlkTU-K23S4xALGuC2JPiBHiNF4AEfrp_c3pcnMd4g9JhFQhRPSuOCcIMMYFPir_v_W8X9DBbNRnvSt-X1rXfv6zKbz-vodR_xqBjzIpxa9OYKZZj8Nb0OmwLlOvKjRl2v-auvDdzQzkSceiQa-OkJl22yrU6nBVHvbJRn-_u0-LHxw_XF58XV18_XV6srhYt5TAtADradZTVDembjqKqUoQwoBWoiiuFk8JB4IaqrqcKY9FxjPu6AqJaIQglp8W7re84NxvdtdpNQVk5BrNR4U56ZeSh4sxaDv6XrIDS5JAMXu8Mgr-ddZzkxsRWW6uc9nOUGABDzTHLvV7-h974Obg0XqJQjTgCxh6oQVktjet96ttmU7lirBI8obntq0fUWis7raO3c951PATfbME2LTgG3e9nAyRzUqS3MidF5qQk_MXjfezh-1yQf6ciuJM</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Wan, Bo</creator><creator>Wu, Hua-Yan</creator><creator>Lv, Dao-Jun</creator><creator>Zhou, Xu-Min</creator><creator>Zhong, Li-Ren</creator><creator>Lei, Bin</creator><creator>Zhang, Shou-Bo</creator><creator>Mao, Xiang-Ming</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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However, the biological function of lncRNA PVT1 remains largely unknown. The aim of the present study was to investigate the effect of lncRNA PVT1 expression on the proliferation and migration of prostate cancer cells. Stably transfected prostate cancer cells with downregulated expression of lncRNA PVT1 were constructed by an efficient siRNA fragment, followed by confirmation by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Proliferation was assessed using CCK-8, colony formation and xenograft assays, and cell migration was evaluated using a wound healing assay. The PathScan
Intracellular Signaling Array kit was utilized to explore the underlying molecular mechanisms of lncRNA PVT1 expression in prostate cancer cells. RT-qPCR results confirmed that the lncRNA PVT1 expression level was successfully knocked down in prostate cancer cells. When lncRNA PVT1 expression was downregulated in prostate cancer cells, proliferation and migration were significantly inhibited, compared with the control lncRNA PVT1 group. Furthermore, PVT1 knockdown decreased the phosphorylation of p38 in DU145 cells. Therefore, the present study demonstrated that lncRNA PVT1 downregulation inhibits the proliferation and migration of prostate cancer cells, and is associated with p38 phosphorylation.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30250582</pmid><doi>10.3892/ol.2018.9305</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
subjects | Androgens Care and treatment Cell cycle Cell growth Cervical cancer Development and progression Genetic aspects Genetic regulation Health aspects Medical research Oncogenes Oncology Ovarian cancer Phosphorylation Prostate cancer Studies Wound healing |
title | Downregulation of lncRNA PVT1 expression inhibits proliferation and migration by regulating p38 expression in prostate cancer |
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