shRNA-mediated RPS15A silencing inhibits U937 acute myeloid leukemia cell proliferation and enhances apoptosis.

Ribosomal protein S15a (RPS15A), which is a component of the 40S ribosomal subunit, is able to promote mRNA/ribosome interaction during the early stage of translation. Previous studies have demonstrated that RPS15A regulates cell growth and is involved in several types of human cancer. The aim of the present study was to investigate the role of RPS15A in acute myeloid leukemia (AML). Lentivirus‑delivered short hairpin RNA (shRNA) was used to silence RPS15A expression in the U937 AML cell line. Subsequently, the effects of RPS15A silencing on cell viability, cell cycle progression and apoptosis were investigated. The results indicated that RPS15A knockdown significantly inhibited cell growth. Furthermore, flow cytometric analysis demonstrated that the majority of U937 cells were arrested in G0/G1 phase and sub‑G1 phase after RPS15A knockdown, as determined using propidium iodide staining. In addition, U937 cells underwent apoptosis in response to RPS15A silencing, as determined using Annexin V/7‑aminoactinomycin D staining. In conclusion, the present study provides novel evidence indicating that RPS15A modulates AML cell growth in vitro, and may be considered a novel therapeutic target for the treatment of AML.