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. 2017 Jun 28;8(37):61944–61957. doi: 10.18632/oncotarget.18734

Figure 5. AKT and ERK were down-stream effectors of SRPK1 in gastric cancer cells.

Figure 5

(A) SRPK1-overexpression significantly elevated the phosphorylation levels of AKT and ERK proteins, whereas SRPK1-KMD showed little effect. (B) The activation function of AKT and ERK by SRPK1 can be impaired upon overexpression of PP2A and DUSP6, respectively. The facilitated effects of SRPK1 on cell proliferation (C) and invasion (D) were also down-regulated by PP2A and DUSP6, indicating the critical role of AKT and ERK in SRPK1-mediated tumor progression.