Esophageal cancer (EC) is one type of aggressive
gastrointestinal cancers. The treatment of EC is challenging. Effective therapeutic targets require development.
Long non-coding RNA TRPM2
antisense RNA (LncRNA TRPM2-AS) is considering a novel
biomarker and therapeutic target for various types of
cancer. However, the role of
lncRNA TRPM2-AS in EC remains unknown. This study aimed to illustrate effects of
LncRNA TRPM2-AS on EC growth and
metastasis and potential underlying molecular mechanisms.
LncRNA TRPM2-AS expression was determined in both EC tissues and cell lines by quantitative real-time polymerase-chain reaction (qRT-PCR). Cell proliferation ability was evaluated by cell counting kit-8 and colony formation assays. Cell apoptosis was analyzed by flow cytometry. Cell migration and invasion were determined using transwell. Epithelial-mesenchymal transition (EMT)-related markers expression were determined using qRT-PCR and Western blotting. Furthermore, potential
lncRNA TRPM2-AS targeting
miRNAs were predicted by public databases. The expression of five selected
miRNAs were validated by qRT-PCR. We found that
lncRNA TRPM2-AS expression was increased in EC tissues and cell lines compared with respective control. Silencing
lncRNA TRPM2-AS suppressed EC cell proliferation, migration, and invasion while promoted cell apoptosis. Moreover,
lncRNA TRPM2-AS knockdown reduced
neural cadherin,
vimentin, and matrix
metallopeptidase 9 gene and
protein expressions while increased
epithelial cadherin expression. Furthermore,
lncRNA TRPM2-AS knockdown promoted
microRNA (miR)-1291, miR-6852-5p, and miR-138-5p expressions. Taken together, this study for the first time demonstrates that upregulation of
lncRNA TRPM2-AS in EC promotes the growth and
metastasis of EC likely through interacting with miR-1291, miR-6852-5p, and miR-138-5p.