MEK2 knockdown increases chemotherapy-induced apoptosis by decreasing pERK levels and increasing levels of p53. Percentage of apoptotic cells upon prednisolone treatment in control NT cells compared to MEK2 knockdown Reh (A) and RS4;11 cells (B). Representative scatter plots of annexin V staining (y-axis) and 7-aminoactinomycin D (7-ADD; x-axis) are shown for NT and MEK2-knockdown cells treated with no drug or 0.8 mM of prednisolone (pred) for 24 hours are shown adjacent to the apoptosis bar graphs. Western blots for pERK, ERK, MEK1, and GR in control NT and in MEK2-knockdown Reh (C) and RS4;11 cell lines (D). Western blots for p53 in control NT and in MEK2-knockdown Reh (E) and RS4;11 cell lines (F) treated with 0.8 mM prednisolone (pred) or 50 nM doxorubicin (doxo) for 24 hours. Cell viability was measured in Reh control NT cells expressing GFP (NT GFP), NT cells expressing dimerization domain dominant-negative p53 (NT DDp53), MEK2-knockdown lines expressing green fluorescent protein (MEK2 KD GFP), or MEK2-knockdown lines expressing dimerization domain dominant-negative p53 (MEK2 KD DDp53); cells were treated with indicated concentrations of doxorubicin (G) or prednisolone (H) for 24 hours. *P ≤ .05. pERK, phosphorylated ERK.