Abstract
Prostate cancer is a common malignancy with a high mortality rate. Long non‑coding RNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) has been reported to serve tumor‑promoting roles. However, the underlying mechanism requires further examination. In the present study, it was demonstrated that MALAT1 was increased while microRNA (miR/miRNA)‑1‑3p was decreased in prostate cancer cell lines. The silencing of MALAT1 inhibited migration, invasion and epithelial‑mesenchymal transition, when epithelial (E)‑cadherin expression level was increased, and neural (N)‑cadherin, vimentin, Slug and Snail expression levels were decreased. Dual‑luciferase reporter assay results demonstrated that miR‑1‑3p bound to MALAT1 and coronin 1C (CORO1C) 3' untranslated region, and MALAT1 competed with CORO1C for the binding sites of miR‑1‑3p. MALAT1 inhibited the expression of miR‑1‑3p and vice versa. MALAT1 knockdown induced the decline of CORO1C, which was subsequently recovered by the miR‑1‑3p inhibitor. In addition, by inhibiting miR‑1‑3p or overexpressing CORO1C, the silencing of MALAT1‑induced phenotypic alterations were restored. In conclusion, MALAT1 serving as a degradable miRNA sponge, may sequester miR‑1‑3p from CORO1C and by silencing MALAT1, migration, invasion and epithelial‑mesenchymal transition may be inhibited in prostate cancer cells. MALAT1 and CORO1C may serve as novel clinical therapeutic targets for prostate cancer.