Downregulation of microRNA‑21 expression inhibits proliferation, and induces G1 arrest and apoptosis via the PTEN/AKT pathway in SKM‑1 cells.

Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis and may progress to acute myeloid leukemia (AML). MicroRNAs (miRNA/miRs) as oncogenes or tumor suppressors regulate a number of biological processes including cell proliferation, cell cycle and apoptosis in different types of cancer cells. Recently, it has been reported that miR‑21 as an oncogene is overexpressed and directly targets SMAD‑7 in MDS. However, little is known about the mechanism of miR‑21 in the progression of MDS. In the present study, the role of miR‑21 in the proliferation and apoptosis of SKM‑1 cells, an acute myeloid leukemia cell line established in the AML/MDS leukemic phase was investigated. The present results demonstrated that downregulation of miR‑21 inhibited proliferation, induced apoptosis and caused G1 phase cell cycle arrest of SKM‑1 cells. In addition, the expression levels of apoptosis regulator Bcl‑2 (bcl2), cyclinD1 and phosphorylated‑protein kinase B (AKT) were significantly decreased in SKM‑1 cells transfected with the miR‑21 inhibitor, whilst the expression levels of phosphatase and tensin homolog (PTEN), bcl‑associated protein X (bax) and cleaved caspase 3 were significantly elevated. Furthermore, knockdown of Akt by small interfering (si)RNA significantly increased the expression of bax, cleaved caspase 3 and reduced the expression of bcl2 and cyclinD1 in SKM‑1 cells. Taken together, these data indicate that miR‑21 targets the PTEN/AKT pathway in the pathogenesis of MDS and could be a potential target for MDS therapy.