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Downregulation of BRAF-activated non-coding RNA suppresses the proliferation, migration and invasion, and induces apoptosis of hepatocellular carcinoma cells
The long non-coding RNA BRAF-activated non-coding RNA (BANCR) has been reported to serve essential roles in the progress of a various cancer types. The purpose of the present study was to investigate the effect of lncRNA BANCR in HCC cells. The expression of BANCR in the HCC cell line Huh7 and a nor...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5649532/ https://www.ncbi.nlm.nih.gov/pubmed/29085476 http://dx.doi.org/10.3892/ol.2017.6770 |
Sumario: | The long non-coding RNA BRAF-activated non-coding RNA (BANCR) has been reported to serve essential roles in the progress of a various cancer types. The purpose of the present study was to investigate the effect of lncRNA BANCR in HCC cells. The expression of BANCR in the HCC cell line Huh7 and a normal liver cell line were determined using reverse transcription-quantitative polymerase chain reaction. The expression of BANCR in Huh7 cells was downregulated by short hairpin (sh)RNA. Subsequently, the proliferation, apoptosis, migration and invasion rates were determined, along with the activity of MAPK/ERK kinase (MEK) and mitogen-activated protein kinase signaling pathways. The results revealed that BANCR was overexpressed in Huh7 cells when compared with normal liver cells. The downregulation of BANCR significantly inhibited the proliferation and colony formation ability, and induced cell cycle arrest and apoptosis of Huh7 cells. The migration and invasion of Huh7 cells were also suppressed in BANCR shRNA-transfected cells. The downregulation of BANCR significantly inhibited the activity of MEK, extracellular signal-regulated kinase and janus kinase signaling pathways. Collectively, these findings demonstrated that the lncRNA BANCR is oncogenic in Huh7 cells, and may be a promising molecular target for HCC therapy. |
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