Fig 2: Western blot analysis revealed that siRNA-mediated RKIP silencing blocked IL-6-induced STAT3 phosphorylation in (A) A549 cells and (B) NCI-H1299 cells. RKIP, Raf kinase inhibitor protein; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription; pSTAT3, phosphorylated signal transducer and activator of transcription 3; siRNA, small interfering RNA.

Fig 3: (A) Western blot analysis of RKIP expression levels in tissue from lymph node metastasis-positive or lymph node metastasis-negative patients with NSCLC. (B) The grayscale density of RKIP protein expression was evaluated using Photoshop software. The comparison of RKIP expression levels between these two sub-groups was analyzed using the Mann-Whitney U-test (*P<0.05; error bars represent the mean + standard deviation). NSCLC, non-small cell lung cancer; RKIP, Raf kinase inhibitor protein.

Fig 4: PEBP1 mediates the activation of the Akt/Bad/Bcl-2 signaling pathway by LINC00473 in Dex-stimulated hBMSCs. The result of western blot analysis revealed (Aa and b) the protein expression levels of PEBP1, p-Akt and Akt in each groups following infection with LINC00473-up lentivirus in Dex-induced hBMSCs (*P<0.05 compared with the Dex group and Dex + Vector group), and (Ba and b) the protein expression levels of PEBP1 and p-Akt in each groups following co-transfection with LINC00473 and PEBP1 in Dex-stimulated hBMSCs (*P<0.05 compared with the Dex + LINC00473-up group and Dex + LINC00473-up + sh-Control group), and (Ca and b) the protein expression levels of PEBP1 and p-Akt in each group following transfection with LINC00473 and PEBP1 respectively in Dex-induced hBMSCs (*P<0.05 compared with the Dex group, Dex + Vector group and Dex + PEBP1-Control group). (D) The results of RT-qPCR revaled the PEBP1 mRNA expression in each groups (*P<0.05 compared with the Dex group and Dex + Vector group, #P<0.05 compared with the Dex + LINC00473-up group, &P<0.05 compared with the Dex group and Dex + PEBP1-Control group). All data are presented as the mean values ± standard deviation 3 three independent experiments. PEBP1, phosphatidylethanolamine-binding protein 1; Akt, protein kinase B; Bad, Bcl-2-associated death promoter; Bcl-2, B-cell lymphoma 2; LINC00473, lncRNA-00473; hBMSCs, human bone marrow-derived mesenchymal stem cells; Dex, dexamethasone; p-Akt, phosphorylated Akt; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.

Fig 5: Efficiency of transfection of hBMSCs with LINC00473 and PEBP1. (A-a) hBMSCs expressing GFP tagged LINC00473-up lentivirus under a fluorescence microscope (scale bar, 1,000 µm) and (A-b) under a light microscope (scale bar, 1,000 µm). The results of RT-qPCR revealed that (A-c) the relative expression of LINC00473 was significantly upregulated by LINC00473-up lentivirus (494%), *P<0.05 compared with the normal group and vector group, and (B-a) the relative expression of PEBP1 was significantly downregulated by 3 shRNAs for PEBP1 (sh-PEBP1), *P<0.05 compared with the normal group and sh-Control group, and (B-b) the relative expression of PEBP1 was a significantly upregulated by PEBP1 overexpression vector (PEBP1-up), *P<0.05 compared with the normal group and PEBP1-Control group. The results of western blot analysis revealed that (C-a) the relative expression of PEBP1 protein was significantly downregulated by the 3 sh-PEBP1, *P<0.05 compared with the normal group and sh-Control group, and (C-b) the relative expression of PEBP1 protein was a significantly upregulated by PEBP1-up, *P<0.05 compared with the normal group and PEBP1-Control group. All data were presented as the means ± standard deviation. hBMSCs, human bone marrow-derived mesenchymal stem cells; LINC00473, lncCRNA-00473; PEBP1, phosphatidylethanol-amine-binding protein 1; GFP, green fluorescent protein; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.