Original Article
Overexpression of the long non-coding RNA BLACAT1 promotes cell proliferation and invasion in colorectal cancer
Abstract
Background: Recent evidence demonstrates that the long non-coding RNA (lncRNA) BLACAT1 is associated with the progression and development of various cancers; however, its effect on tumorigenesis of colorectal cancer (CRC) is still poorly understood. The aim of the present study was to investigate the expression and function of BLACAT1 in CRC.
Methods: Expression data from the GEO and GEPIA databases and results obtained from clinical samples/ patients were used to determine the correlation between BLACAT1 expression, and CRC metastasis and overall survival (OS). Furthermore, we knocked down BLACAT1 using short interfering RNA (siRNA) and observed its biological functions using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), cell counting kit-8 (CCK-8) assay, tumor cell clone formation, and Matrigel invasion assays in the HCT116 cell line.
Results: BLACAT1 level was higher in CRC tissues and cell lines than in normal colon mucosal tissues and cell lines. Correlation of data from the GEO and GEPIA databases with several clinical parameters revealed that CRC patients with high BLACAT1 expression showed poor OS. Multivariate analysis indicated that high BLACAT1 expression is an independent risk factor in patients with CRC. Furthermore, siRNA-mediated knockdown of BLACAT1 suppressed proliferation and invasion of CRC cells in vitro. This in turn was associated with reduced expression of cyclin D1, CDK6, and vimentin, and enhanced expression of E-cadherin.
<Conclusions: BLACAT1 may play an important role in the progression and development of CRC, and may serve as a potential therapeutic target for patients with CRC.
Methods: Expression data from the GEO and GEPIA databases and results obtained from clinical samples/ patients were used to determine the correlation between BLACAT1 expression, and CRC metastasis and overall survival (OS). Furthermore, we knocked down BLACAT1 using short interfering RNA (siRNA) and observed its biological functions using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), cell counting kit-8 (CCK-8) assay, tumor cell clone formation, and Matrigel invasion assays in the HCT116 cell line.
Results: BLACAT1 level was higher in CRC tissues and cell lines than in normal colon mucosal tissues and cell lines. Correlation of data from the GEO and GEPIA databases with several clinical parameters revealed that CRC patients with high BLACAT1 expression showed poor OS. Multivariate analysis indicated that high BLACAT1 expression is an independent risk factor in patients with CRC. Furthermore, siRNA-mediated knockdown of BLACAT1 suppressed proliferation and invasion of CRC cells in vitro. This in turn was associated with reduced expression of cyclin D1, CDK6, and vimentin, and enhanced expression of E-cadherin.
<Conclusions: BLACAT1 may play an important role in the progression and development of CRC, and may serve as a potential therapeutic target for patients with CRC.
