Silencing of MALAT1 inhibits migration and invasion by sponging miR‑1‑3p in prostate cancer cells.

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.