Fig. 4: SQS activates the Src and ERK pathways in lung cancer cells.
From: Squalene synthase promotes the invasion of lung cancer cells via the osteopontin/ERK pathway
a CL1-0 cells infected with the vector and SQS overexpression plasmid were subjected to western blot analyses of SQS, pSrc, Src, pERK, ERK, pAKT473, AKT and α-tubulin levels. b Comparison of pSrc, Src, pERK, ERK, pAKT473, and AKT levels between SQS knockdown A549 and CL1-5 cells and nonsilenced shRNA control cells. c Western blots showing the levels of pSrc, Src, pERK, ERK, pAKT473, AKT and α-tubulin in CL1-0/SQS cells after treatment with Src kinase inhibitor-1 (SKI, 10 μM). d Heatmap showing the protein levels of AKT, AKT_pS473, Src, and Src_pY416 and migration ability in the lung cancer cell panel. e Plot showing the correlations between the protein levels of AKT_pS473 protein/Src_pY416 protein and migration in the lung cancer cell panel. f CL1-0/SQS cells were treated with or without DMSO, Src inhibitor-1 (SKI) (10 μM), PD98059 (20 μM) and LY294002 (10 μM). Top panel, The total protein samples were subjected to western blot analyses of SQS and α-tubulin levels (cell extract, CE). Middle panel, MMP1 protein expression levels from condition medium (CM). Bottom panel, Invasion (open) and migration (filled) of CL1-0/SQS cells treated with DMSO, SKI, PD98059 and LY294002 compared to CL1-0/Vector cells. Data are presented as the means ± SDs. **P < 0.01. g CL1-0/SQS cells were treated with or without MβCD (10 mM) for 30 min 37 °C. Western blot analyses of SQS, pSrc, pERK and pAKT and α-tubulin levels of CL1-0/SQS cells. h Effect of cholesterol replenishment on the phosphorylation of Src, ERK, and AKT in CL1-0 cells.
