RGS20 Promotes Tumor Progression through Modulating PI3K/AKT Signaling Activation in Penile Cancer

Figure 6

The overexpression of constitutively active PI3K p110α rescued malignant phenotypes impaired by RGS20 depletion. (a) Western blotting analysis on the expression of PI3K/AKT signaling pathway proteins after transfection with empty vector (EV), PI3K p110α Myr, or PI3K p110α KD plasmids in RGS20-depleted 149RM and Penl1cells. (b) CCK-8 analysis on cell viability after PI3K p110α Myr and KD plasmids transfection in RGS20-depleted 149RM and Penl1 cells. The cell viability in Scr control was regards as 100%. , , as compared with EV. (c) Soft agar assay on clonogenesis after PI3K p110α Myr and KD plasmids transfection in RGS20-depleted 149RM and Penl1 cells. The soft agar clonogenesis in Scr control was regards as 100%. , , as compared with EV. (d) Caspase-3 activity after PI3K p110α Myr and KD plasmid transfection in RGS20-depleted 149RM and Penl1 cells. The caspase-3 activity in Scr control was regards as 100%. , , as compared with EV. (e) Wound healing assay on PC cells following PI3K p110α Myr and KD plasmid transfection in RGS20-depleted 149RM and Penl1 cells. Bars: 100 μm. The cell migration in Scr control was regards as 100%. , , as compared with EV. (f) Transwell invasion assay on PC cells following PI3K p110α Myr and KD plasmid transfection in RGS20-depleted 149RM and Penl1 cells. Bars: 50 μm. The cell invasion in Scr control was regards as 100%. , , as compared with EV.

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