Long non-coding RNA BLACAT1 promotes cell proliferation, migration and invasion in cervical cancer through activation of Wnt/β-catenin signaling pathway.

Abstract

Long noncoding RNAs (lncRNAs) are aberrantly expressed in various cancers. The purpose of this study was to determine the association of lncRNA (BLACAT1) with the prognosis of cervical cancer (CC) patients, and to further investigate the potential mechanisms of BLACAT1 function in CC progression. The expressions of BLACAT1 in CC tissues and cells were estimated by quantitative Real-time polymerase chain reaction (qRT-PCR). We compared the expression of BLACAT1 with the clinicopathological characteristics and survival of CC patients. MTT, colony formation, and transwell assay were performed to explore the effects of BLACAT1 expression on growth, migration, and invasion of CC cells. Protein levels of β-catenin and MMP-7 were evaluated by Western blotting. We found that BLACAT1 expression was significantly increased in CC tissues and cells lines. In addition, the expression level of BLACAT1 was positively correlated with distant metastasis (p=0.001), FIGO stage (p=0.010), and histological grade (p=0.012). Moreover, patients with high BLACAT12 expression had shorter overall survival and progression-free survival time than those with low BLACAT1 expression, with the data provided by multivariate analysis suggesting that BLACAT1 expression could serve as an independent prognostic factor in CC patients. Functionally, in vitro assay indicated that down-regulation of BLACAT1 significantly suppressed CC cells proliferation, migration, and invasion. Mechanistically, the results of Western blot showed that the expression of β-catenin and MMP-7 was significantly down-regulated in CC cells transfected with si-BLACAT1. These findings suggested that BLACAT1, as a novel prognostic biomarker, might be an oncogenic lncRNA which promoted proliferation, migration, and invasion by modulating Wnt/β-catenin signaling. Our results enlarged our knowledge in the molecular pathology of CC tumorigenesis.