Silencing of Long Noncoding RNA SNHG6 Inhibits Esophageal Squamous Cell Carcinoma Progression via miR-186-5p/HIF1α Axis.

AIMS

Long noncoding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) has been shown to be upregulated in esophageal squamous cell carcinoma (ESCC). However, its detailed function in ESCC remains unknown. We investigated its specific roles in ESCC cell proliferation, invasion, and migration.

METHODS

Gene expression was evaluated by quantitative reverse transcriptase polymerase chain reaction and western blot. The subcellular localization of lncRNA SNHG6 was determined using subcellular location assay. Luciferase reporter assay and RNA pull-down assay were applied to determine the interaction between lncRNA SNHG6, miR-186-5p, and hypoxia-inducible factor 1α (HIF1α). The cell proliferation, migration, and invasion abilities were evaluated by using cell count kit-8, colony formation assay, and transwell migration and invasion assays.

RESULTS

LncRNA SNHG6 and HIF1α were upregulated, while miR-186-5p was downregulated in ESCC tissues and cell lines. Knockdown of lncRNA SNHG6 inhibits ESCC cell proliferation, migration, and invasion. A negative correlation between lncRNA SNHG6 and miR-186-5p expression was found in ESCC tissues. Similarly, there is a positive correlation between lncRNA SNHG6 and HIF1α expression in ESCC tissues. Conversely, miR-186-5p expression was negatively correlated with HIF1α expression in ESCC tissues. Furthermore, lncRNA SNHG6 was identified as a decoy for miR-186-5p, thereby promoting the expression of miR-186-5p target HIF1α. More significantly, restoration of SNHG6 or HIF1α could reverse the inhibitory effect of miR-186-5p on ESCC cell proliferation, migration, and invasion.

CONCLUSIONS

Downregulation of SNHG6 inhibited the proliferation, migration, and invasion of ESCC cells through regulating miR-186-5p/HIF1α axis, providing a novel therapeutic target for ESCC.