SRPK1‑siRNA suppresses K562 cell growth and induces apoptosis via the PARP‑caspase3 pathway

Abstract

Serine-arginine protein kinase1 (SRPK1) has been used as an important signal mediator, and is associated with cancer development. However, studies have yet to determine whether SRPK1 suppresses leukemia cell growth and induces apoptosis. Studies have also yet to reveal the underlying mechanisms. In the present study, the effects of downregulating SRPK1 gene expression on chronic myeloid leukemia cell lines (K562cells) were investigated through RNA interference (RNAi) and the proliferation inhibition and apoptosis induction of SRPK1 in K562 cells were analyzed. K562 cells were transfected with two different concentrations of siRNA, and the transfection efficiency was detected via flow cytometry. The expression of SRPK1 was detected via reverse transcription‑quantitative polymerase chain reaction. K562 cell proliferation and apoptosis were analyzed using MTT and flow cytometry respectively. The roles of caspase‑3, poly(ADP‑ribose) polymerase (PARP), p53 and B-cell lymphoma (Bcl)‑2/Bcl‑2 associated X, apoptosis regulator (Bax) proteins in the apoptosis of human K562 cells were further examined through western blot analysis. The SRPK1 expression was lower in the K562cells transfected with SRPK1‑siRNA compared with untransfected cells. The inhibition rate in the transfected groups was increased compared with the untransfected groups. Compared with control groups, the number of apoptotic cells in the SRPK1‑silenced groups increased. The number of early apoptotic cells also increased. The cleaved caspase‑3, cleaved PARP and p53 expression levels were significantly increased in the RNAi groups compared with control groups. Conversely, the Bcl‑2/Bax rate was significantly lower. In conclusion, the knockdown of the SRPK1 gene by RNAi inhibited the proliferation of K562cells and induced their apoptosis. Apoptosis was induced by the activation of the PARP‑caspase3 pathway.