Esophageal squamous cell carcinoma (ESCC) is an intractable esophageal cancer caused by smoking, alcohol consumption and nutritional deficiencies. Recently, long non-coding RNA SET-binding factor 2 antisense RNA 1 (SBF2-AS1) was validated as an oncogene in multiple cancers. However, the mechanism of SBF2-AS1 in ESCC progression is poorly understood. In the present research, we found that the expression of SBF2-AS1 and PFN2 was up-regulated, while miR-494 was down-regulated in ESCC tumors and cells using quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and transwell assay demonstrated that silencing of SBF2-AS1 suppressed proliferation, migration and invasion. Moreover, western blot showed that SBF2-AS1 deletion also inhibited epithelial to mesenchymal transition (EMT) by detecting MMP9, Vimentin and E-cadherin protein expression. We confirmed that miR-494 was a target of SBF2-AS1 by luciferase reporter system, RIP and RNA pull-down assay. In addition, miR-494 inhibitor reversed the repression induced by SBF2-AS1 silencing on ESCC cell proliferation, migration, invasion and EMT. Furthermore, PFN2 was negatively regulated by miR-494. Besides, restoration of PFN2 inversed the inhibition effects on cell proliferation, migration, invasion and EMT induced by SBF2-AS1 silencing in ESCC. In conclusion, SBF2-AS1 contributed to cell proliferation, migration, invasion and EMT in ESCC by enhancing PFN2 expression via sponging miR-494, providing promising biomarkers for ESCC diagnosis and treatment.
Overexpression of long non-coding RNA SBF2-AS1 promotes cell progression in esophageal squamous cell carcinoma (ESCC) by repressing miR-494 to up-regulate PFN2 expression
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Qiu Zhang, Xixiang Pan, Dongyang You; Overexpression of long non-coding RNA SBF2-AS1 promotes cell progression in esophageal squamous cell carcinoma (ESCC) by repressing miR-494 to up-regulate PFN2 expression. Biol Open 2020; bio.048793. doi: https://doi.org/10.1242/bio.048793
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