[No authors listed]
Long nonâcoding 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 cancerâassociated nonâcoding RNA (PRNCR)1â2 in breast cancer. The expression levels of PRNCR1â2 were detected in breast cancer tissues and numerous breast cancer cell lines using reverse transcriptionâquantitative polymerase chain reaction. Depletion of PRNCR1â2 expression in breast cancer cells was conducted through small interfering RNAâmediated 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 kinase 2 (CHK2), protein kinase B (AKT), phosphorylated (p)âCHK2 and pâAKT were measured by western blotting. The results demonstrated that PRNCR1â2 expression was significantly elevated in breast cancer tissues compared with in adjacent normal tissues. Furthermore, depletion of PRNCR1â2 in HSâ578T and MDAâMBâ231 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, PRNCR1â2 depletion increased CHK2 phosphorylation and decreased AKT phosphorylation in HSâ578T and MDAâMBâ231 cells. In conclusion, the lncRNA PRNCR1â2 may promote breast cancer cell proliferation, migration, invasion and cell cycle progression.
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