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LncRNA SBF2-AS1 promotes hepatocellular carcinoma metastasis by regulating EMT and predicts unfavorable prognosis.
OBJECTIVE: Recent studies have furthered our understanding of the function of long noncoding RNAs (lncRNAs) in numerous biological processes, including cancer. The present study aimed to investigate the expression of lncRNA SBF2-AS1 (SBF2-AS1) in patients with hepatocellular carcinoma (HCC) and to investigate its effect on HCC cells.
PATIENTS AND METHODS: Using quantitative reverse transcription-polymerase chain reaction, we detected SBF2-AS1 expression in HCC cell lines and primary tumor tissues. The associations between SBF2-AS1 expression and the clinicopathological factors and outcome of HCC patients were statistically analyzed. MTT assay and transwell assay were performed to determine the proliferation, migration and invasion, respectively. In addition, we evaluated the activation of Mesenchymal-epithelial transition (EMT) pathway by Western blot.
RESULTS: We found that SBF2-AS1 expression levels were significantly up-regulated in HCC tissues and cell lines compared with the corresponding noncancerous liver tissues and normal hepatic cell line. In addition, high SBF2-AS1 expression levels were correlated with vein invasion (p = 0.008) and TNM stage (p = 0.013). Furthermore, Kaplan-Meier survival analysis indicated that high expressions of SBF2-AS1 were correlated with shorter overall survival of HCC patients. Univariate and multivariate analysis identified high SBF2-AS1 expression as an unfavorable prognostic factor for overall survival. Further functional analysis demonstrated that knockdown of SBF2-AS1 significantly inhibited HCC cells proliferation, migration and invasion. Mechanistically, we found that SBF2-AS1 could promote the activation of EMT pathway, which was demonstrated by measuring the expression levels of EMT-related markers.
CONCLUSIONS: SBF2-AS1 might be considered as a novel molecule involved in HCC development, which provides a potential therapeutic target for HCC.
PATIENTS AND METHODS: Using quantitative reverse transcription-polymerase chain reaction, we detected SBF2-AS1 expression in HCC cell lines and primary tumor tissues. The associations between SBF2-AS1 expression and the clinicopathological factors and outcome of HCC patients were statistically analyzed. MTT assay and transwell assay were performed to determine the proliferation, migration and invasion, respectively. In addition, we evaluated the activation of Mesenchymal-epithelial transition (EMT) pathway by Western blot.
RESULTS: We found that SBF2-AS1 expression levels were significantly up-regulated in HCC tissues and cell lines compared with the corresponding noncancerous liver tissues and normal hepatic cell line. In addition, high SBF2-AS1 expression levels were correlated with vein invasion (p = 0.008) and TNM stage (p = 0.013). Furthermore, Kaplan-Meier survival analysis indicated that high expressions of SBF2-AS1 were correlated with shorter overall survival of HCC patients. Univariate and multivariate analysis identified high SBF2-AS1 expression as an unfavorable prognostic factor for overall survival. Further functional analysis demonstrated that knockdown of SBF2-AS1 significantly inhibited HCC cells proliferation, migration and invasion. Mechanistically, we found that SBF2-AS1 could promote the activation of EMT pathway, which was demonstrated by measuring the expression levels of EMT-related markers.
CONCLUSIONS: SBF2-AS1 might be considered as a novel molecule involved in HCC development, which provides a potential therapeutic target for HCC.
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