BACKGROUND

Accumulating evidence indicates dysregulated expression of the long non-coding RNA HOTAIR (lncRNA-HOTAIR) may play a significant role in tumor progression. LncRNA-HOTAIR promotes several processes in esophageal cancer (EC), including cell growth, differentiation, invasion and migration. However, the mechanisms by which lncRNA-HOTAIR promotes invasion and migration EC remain unclear.

METHODS

LncRNA-HOTAIR and miR-148a expression were quantified in 40 paired human EC and tumor-adjacent tissues and EC cell lines by quantitative real-time PCR (qRT-PCR). The CCK8 assay was used to quantify cell proliferation. Transwell invasion and migration assays were performed to assess cell invasion and migration. Western blot analysis was used to quantify E-cadherin, N-cadherin, Vimentin, and Snail2 expression. StarBase V2.0 was used to identify putative miRNA binding sites in lncRNA-HOTAIR; luciferase reporter assays were performed to validate the function of the predicted binding sites.

RESULT

High lncRNA-HOTAIR expression was associated with significantly poorer overall survival in EC. In vitro analysis showed lncRNA-HOTAIR enhanced EC cell proliferation, invasion and migration, and promoted the EMT. Mechanistic investigations revealed lncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression.

CONCLUSIONS

LncRNA-HOTAIR acts as a miR-148a sponge to positively regulate Snail2 expression, enhance cell invasion and metastasis, and promote the EMT in EC. LncRNA-HOTAIR may play an important role in tumor development and progression and represent a novel therapeutic target for EC.