LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma.

BACKGROUND

The long non-coding RNA (lncRNA) SNHG6 was significantly upregulated in esophageal squamous-cell carcinoma (ESCC), and it promoted ESCC cell proliferation, invasion, and migration. However, the effects of SNHG6 on cell apoptosis and the corresponding underlying mechanisms have not yet reported.

METHODS

Apoptosis was detected by flow cytometric analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used for mRNA and protein quantification, respectively. A luciferase reporter assay was performed to verify downstream target genes for SNHG6 and miR-101-3p.

RESULTS

Dysregulation of SNHG6 inhibited apoptosis in ESCC cells and regulated the expression of apoptosis-related proteins such as Bcl-2, Mcl-1, Bax and Caspase-3. Functionally, miR-101-3p could compete binding with 3'-untranslated region of SNHG6 and downregulation of miR-101-3p reversed its effect on cell apoptosis in SNHG6 knockdown cells. was confirmed as a downstream target gene of miR-101-3p, silencing expression had the same effect on apoptosis and protein expression as knocking down SNHG6. Overexpression of reversed the effects of miR-101-3p overexpression on cell apoptosis in ESCC cells.

CONCLUSION

In this study, we found that upregulation of the lncRNA SNHG6 inhibited apoptosis via miR-101-3p/ axis in ESCC. These findings may contribute to the diagnosis and treatment of ESCC.