The novel long non‑coding RNA PRNCR1‑2 is involved in breast cancer cell proliferation, migration, invasion and cell cycle progression.

Abstract

Long non‑coding RNAs (lncRNAs) have recently been reported to act as important mediators of tumor initiation and progression. The present study aimed to investigate the expression and pathogenic roles of the lncRNA prostate cancer‑associated non‑coding RNA (PRNCR)1‑2 in breast cancer. The expression levels of PRNCR1‑2 were detected in breast cancer tissues and numerous breast cancer cell lines using reverse transcription‑quantitative polymerase chain reaction. Depletion of PRNCR1‑2 expression in breast cancer cells was conducted through small interfering RNA‑mediated silencing. Subsequently, cell proliferation was assessed by MTS assay, cell migration and invasion capacities were evaluated using the Transwell culture system, and cell cycle progression and apoptosis were analyzed by flow cytometry. Protein expression levels of the signaling components checkpoint kinase2 (CHK2), protein kinaseB (AKT), phosphorylated (p)‑CHK2 and p‑AKT were measured by western blotting. The results demonstrated that PRNCR1‑2 expression was significantly elevated in breast cancer tissues compared with in adjacent normal tissues. Furthermore, depletion of PRNCR1‑2 in HS‑578T and MDA‑MB‑231 breast cancer cells markedly suppressed their proliferation rates, migration and invasion capacities, and cell cycle progression; however, it had no effect on cell apoptosis. In addition, PRNCR1‑2 depletion increased CHK2 phosphorylation and decreased AKT phosphorylation in HS‑578T and MDA‑MB‑231 cells. In conclusion, the lncRNA PRNCR1‑2 may promote breast cancer cell proliferation, migration, invasion and cell cycle progression.