RANKL knockdown suppresses the PI3K/AKT pathway in A549/DPP cells. (A) Representative immunoblots for (A) p-PI3K, PI3K, p-AKT, AKT, p-stat3 and stat3 and quantitative assessments of the concentration of (B) p-PI3K/PI3K, (C) p-AKT/AKT and (D) p-stat3/stat3 in A549/DPP cells following temporary transfection with si-Control or si-lncRNA RANKL for 24 h. (E) Representative immunoblots for (A) p-PI3K, PI3K, p-AKT, AKT, p-stat3 and stat3 and quantitative assessments of the concentration of (F) p-PI3K/PI3K, (G) p-AKT/AKT and (H) p-stat3/stat3 (H) in A549/DPP cells following temporary transfection with a NC or lncRNA RANKL for 24 h. Data are presented as mean ± standard error of the mean. *P<0.05, **P<0.01. RANKL, receptor activator of nuclear factor-κ B ligand; p-, phosphorylated; PI3K, phosphatidylinositol 3-kinase; AKT, protein kinase B; DPP, cisplatin; stat3, signal transducer and activator of transcription 3; si, short interfering; lncRNA, long non-coding RNA; NC, negative control.