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Long non-coding RNA EGFR-AS1 sponges micorRNA-381 to upregulate ROCK2 in bladder cancer
The present study aimed to investigate the role of the long non-coding RNA EGFR-AS1 in bladder cancer (BC). In this study gene expression of both BC and non-tumor tissues from BC patients were measured by quantitative PCR. Cell transfections were performed to analyze gene interactions in HT-1197 cel...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7039139/ https://www.ncbi.nlm.nih.gov/pubmed/32194685 http://dx.doi.org/10.3892/ol.2020.11283 |
Sumario: | The present study aimed to investigate the role of the long non-coding RNA EGFR-AS1 in bladder cancer (BC). In this study gene expression of both BC and non-tumor tissues from BC patients were measured by quantitative PCR. Cell transfections were performed to analyze gene interactions in HT-1197 cells. Transwell assays were performed to analyze cell invasion and migration of HT-1197 cells. It was revealed that epidermal growth factor receptor-antisense RNA 1 (EGFR-AS1) was upregulated in BC and positively associated with rho associated coiled-coil containing protein kinase 2 (ROCK2). Analysis of data collected in follow-ups indicated that EGFR-AS1 expression was significantly associated with poorer overall survival of patients with BC. Moreover, in bladder cancer cells, EGFR-AS1 overexpression mediated the upregulation of ROCK2, while microRNA (miR)-381 mediated the downregulation of ROCK2. However, EGFR-AS1 and ROCK2 failed to affect each other. Bioinformatics analysis indicated that miR-381 binds EGFR-AS1. In addition, EGFR-AS1 and ROCK2 overexpression resulted in the promotion of cell invasiveness and migration of HT-1197 BC cells. Conversely, miR-381 was revealed to partially reverse the effect of EGFR-AS1 overexpression. Therefore, EGFR-AS1 may sponge miR-381 to upregulate ROCK2 in BC, thereby promoting cell invasion and migration. |
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