Cargando…
LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer
Accumulating evidence indicates that the aberrant expression of long noncoding RNAs (lncRNAs) is involved in tumorigenesis and cancer development. However, the biological functions and underlying mechanisms of lncRNAs in bladder cancer (BC) remain largely unknown. Here, we analyzed the lncRNA and mR...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163378/ https://www.ncbi.nlm.nih.gov/pubmed/30149689 http://dx.doi.org/10.3390/ijms19092531 |
_version_ | 1783359346754715648 |
---|---|
author | Chi, Hong Yang, Rui Zheng, Xiaying Zhang, Luyu Jiang, Rong Chen, Junxia |
author_facet | Chi, Hong Yang, Rui Zheng, Xiaying Zhang, Luyu Jiang, Rong Chen, Junxia |
author_sort | Chi, Hong |
collection | PubMed |
description | Accumulating evidence indicates that the aberrant expression of long noncoding RNAs (lncRNAs) is involved in tumorigenesis and cancer development. However, the biological functions and underlying mechanisms of lncRNAs in bladder cancer (BC) remain largely unknown. Here, we analyzed the lncRNA and mRNA expression profiles in BC using a microarray assay. We found that lncRNA RP11-79H23.3 and phosphatase and tensin homolog (PTEN) were significantly downregulated in BC tissues and cells. Meanwhile, RP11-79H23.3 expression was negatively correlated with clinical stage in BC. Functionally, we found that overexpression of RP11-79H23.3 could suppress cell proliferation, migration, and cell cycle progression, rearrange the cytoskeleton, and induce apoptosis in vitro. Moreover, upregulation of RP11-79H23.3 inhibited the angiogenesis, tumorigenesis, and lung metastasis in vivo, whereas RP11-79H23.3 knockdown exerted a contrary role. Mechanistically, we identified that RP11-79H23.3 could directly bind to miR-107 and abolish the suppressive effect on target gene PTEN, which leads to inactivation of the PI3K/Akt signaling pathway. Taken together, we first demonstrated that RP11-79H23.3 might suppress the pathogenesis and development of BC by acting as a sponge for miR-107 to increase PTEN expression. Our research revealed that RP11-79H23.3 could be a potential target for diagnosis and therapy of BC. |
format | Online Article Text |
id | pubmed-6163378 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-61633782018-10-10 LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer Chi, Hong Yang, Rui Zheng, Xiaying Zhang, Luyu Jiang, Rong Chen, Junxia Int J Mol Sci Article Accumulating evidence indicates that the aberrant expression of long noncoding RNAs (lncRNAs) is involved in tumorigenesis and cancer development. However, the biological functions and underlying mechanisms of lncRNAs in bladder cancer (BC) remain largely unknown. Here, we analyzed the lncRNA and mRNA expression profiles in BC using a microarray assay. We found that lncRNA RP11-79H23.3 and phosphatase and tensin homolog (PTEN) were significantly downregulated in BC tissues and cells. Meanwhile, RP11-79H23.3 expression was negatively correlated with clinical stage in BC. Functionally, we found that overexpression of RP11-79H23.3 could suppress cell proliferation, migration, and cell cycle progression, rearrange the cytoskeleton, and induce apoptosis in vitro. Moreover, upregulation of RP11-79H23.3 inhibited the angiogenesis, tumorigenesis, and lung metastasis in vivo, whereas RP11-79H23.3 knockdown exerted a contrary role. Mechanistically, we identified that RP11-79H23.3 could directly bind to miR-107 and abolish the suppressive effect on target gene PTEN, which leads to inactivation of the PI3K/Akt signaling pathway. Taken together, we first demonstrated that RP11-79H23.3 might suppress the pathogenesis and development of BC by acting as a sponge for miR-107 to increase PTEN expression. Our research revealed that RP11-79H23.3 could be a potential target for diagnosis and therapy of BC. MDPI 2018-08-26 /pmc/articles/PMC6163378/ /pubmed/30149689 http://dx.doi.org/10.3390/ijms19092531 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Chi, Hong Yang, Rui Zheng, Xiaying Zhang, Luyu Jiang, Rong Chen, Junxia LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer |
title | LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer |
title_full | LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer |
title_fullStr | LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer |
title_full_unstemmed | LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer |
title_short | LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer |
title_sort | lncrna rp11-79h23.3 functions as a competing endogenous rna to regulate pten expression through sponging hsa-mir-107 in the development of bladder cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163378/ https://www.ncbi.nlm.nih.gov/pubmed/30149689 http://dx.doi.org/10.3390/ijms19092531 |
work_keys_str_mv | AT chihong lncrnarp1179h233functionsasacompetingendogenousrnatoregulateptenexpressionthroughsponginghsamir107inthedevelopmentofbladdercancer AT yangrui lncrnarp1179h233functionsasacompetingendogenousrnatoregulateptenexpressionthroughsponginghsamir107inthedevelopmentofbladdercancer AT zhengxiaying lncrnarp1179h233functionsasacompetingendogenousrnatoregulateptenexpressionthroughsponginghsamir107inthedevelopmentofbladdercancer AT zhangluyu lncrnarp1179h233functionsasacompetingendogenousrnatoregulateptenexpressionthroughsponginghsamir107inthedevelopmentofbladdercancer AT jiangrong lncrnarp1179h233functionsasacompetingendogenousrnatoregulateptenexpressionthroughsponginghsamir107inthedevelopmentofbladdercancer AT chenjunxia lncrnarp1179h233functionsasacompetingendogenousrnatoregulateptenexpressionthroughsponginghsamir107inthedevelopmentofbladdercancer |