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. 2018 Sep 25;7(12):e1502130. doi: 10.1080/2162402X.2018.1502130

Figure 3.

Figure 3.

SphK1 promotes ccRCC progression by regulating the Akt/mTOR pathway.

Cell viability was measured by MTT assay at 0, 24, 48 and 72 hours in 786-O cells with overexpression of SphK1 or control vector. The data are presented as the means ± S.D. from three independent experiments. B. Representative images of clonogenic assays of 786-O and Caki-1 cells with overexpression of SphK1 or control vector. * < 0.05, ** < 0.01. The colonies were counted and captured. C. Representative images of migration and invasion assays in 786-O cells with overexpression of SphK1 or control vector. Scale bar = 100 μm. D. Downstream effectors of SphK1 were identified by phosphoprotein microarray. The bar chart indicates that phosphorylation levels were downregulated or upregulated by more than 20%. E. Expression of phosphorylation of Akt, mTOR and ERK genes were validated by western blotting. GAPDH was used as a loading control. F. Schematic diagram of the molecular events for SphK1’s function as a oncogene through regulating cell cycle, proliferation, apoptosis and migration effectors.