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Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway

More and more studies have shown that long non-coding RNAs (lncRNAs) play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. LncRNA long intergenic noncoding RNA 00511 (linc00511) is one of the lncRNAs highly express...

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Detalles Bibliográficos
Autores principales: Li, Jun, Li, Yan, Meng, Fandong, Fu, Liye, Kong, Chuize
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131201/
https://www.ncbi.nlm.nih.gov/pubmed/30042171
http://dx.doi.org/10.1042/BSR20171701
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author Li, Jun
Li, Yan
Meng, Fandong
Fu, Liye
Kong, Chuize
author_facet Li, Jun
Li, Yan
Meng, Fandong
Fu, Liye
Kong, Chuize
author_sort Li, Jun
collection PubMed
description More and more studies have shown that long non-coding RNAs (lncRNAs) play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. LncRNA long intergenic noncoding RNA 00511 (linc00511) is one of the lncRNAs highly expressed in bladder cancer tissues and cells. However, little is known about the roles and mechanisms of linc00511 in bladder cancer. Here, we demonstrated that linc00511 was highly expressed in bladder cancer tissues and cells. Linc00511 knockdown could cause the cell proliferation suppression and cell cycle arrest, which were mediated by p18, p21, CDK4, cyclin D1 and phosphorylation Rb. Suppressed linc00511 could induce the apoptosis in T24 and BIU87 cells via activating the caspase pathway. Down-regulation of linc00511 could also suppress the migration and invasion of T24 and BIU87 cells. In addition, we found that the expression of linc00511 was negatively correlated with that of miR-15a-3p in the clinical bladder cancer samples. Further mechanistic studies showed that linc00511 knockdown induced proliferation inhibition, and apoptosis increase might be regulated through suppressing the activities of Wnt/β-catenin signaling pathway. Thus, we revealed that knockdown of linc00511 suppressed the proliferation and promoted apoptosis of bladder cancer cells through suppressing the activities of Wnt/β-catenin signaling pathway. Moreover, we suggested that linc00511 could be a potential therapeutic target and novel biomarker in bladder cancer.
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spelling pubmed-61312012018-09-12 Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway Li, Jun Li, Yan Meng, Fandong Fu, Liye Kong, Chuize Biosci Rep Research Articles More and more studies have shown that long non-coding RNAs (lncRNAs) play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. LncRNA long intergenic noncoding RNA 00511 (linc00511) is one of the lncRNAs highly expressed in bladder cancer tissues and cells. However, little is known about the roles and mechanisms of linc00511 in bladder cancer. Here, we demonstrated that linc00511 was highly expressed in bladder cancer tissues and cells. Linc00511 knockdown could cause the cell proliferation suppression and cell cycle arrest, which were mediated by p18, p21, CDK4, cyclin D1 and phosphorylation Rb. Suppressed linc00511 could induce the apoptosis in T24 and BIU87 cells via activating the caspase pathway. Down-regulation of linc00511 could also suppress the migration and invasion of T24 and BIU87 cells. In addition, we found that the expression of linc00511 was negatively correlated with that of miR-15a-3p in the clinical bladder cancer samples. Further mechanistic studies showed that linc00511 knockdown induced proliferation inhibition, and apoptosis increase might be regulated through suppressing the activities of Wnt/β-catenin signaling pathway. Thus, we revealed that knockdown of linc00511 suppressed the proliferation and promoted apoptosis of bladder cancer cells through suppressing the activities of Wnt/β-catenin signaling pathway. Moreover, we suggested that linc00511 could be a potential therapeutic target and novel biomarker in bladder cancer. Portland Press Ltd. 2018-08-29 /pmc/articles/PMC6131201/ /pubmed/30042171 http://dx.doi.org/10.1042/BSR20171701 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Articles
Li, Jun
Li, Yan
Meng, Fandong
Fu, Liye
Kong, Chuize
Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway
title Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway
title_full Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway
title_fullStr Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway
title_full_unstemmed Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway
title_short Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway
title_sort knockdown of long non-coding rna linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing wnt/β-catenin signaling pathway
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131201/
https://www.ncbi.nlm.nih.gov/pubmed/30042171
http://dx.doi.org/10.1042/BSR20171701
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