Fig. 7
HDAC inhibitors upregulate MKP1 in glioma cells and sensitizes to temozolomide treatment. a MKP1 mRNA levels were studied in U87 and GNS166 cell lines under 24 h of treatment with increasing doses of TSA (0.1, 0.5, and 1 µM) and b SAHA (0.1, 0.5, and 1 µM). MKP1 levels were assayed by qRT-PCR data, are normalized to GAPDH expression, and are relative to non-treated cells. c Quantification of oncospheres forming capacity in TSA- and SAHA-treated U87 cells after 7 days in culture. The numbers are relative to control cells (n = 3). d Quantification of P-H3+ cells in TSA- and SAHA GNS166-treated cells (n = 3). e Expression of MKP1 in U87 derived oncospheres in the presence of indicated concentrations of HDAC inhibitors. Levels are relative to non-treated cells (n = 3). f U87 cells were co-transfected with pGL3-MKP1 luciferase promoter construct and increasing doses of TSA (control (0), 0.25, and 0.5 µM) for 48 H. Levels are relative to control condition (n = 3). g Oncosphere formation after 7 days with 0.1 and 0.5 μM SAHA, 50 μM TMZ, or the combination of both compounds. h Cell viability comparing control and MKP1-overexpressing U87 cells cultured with 0.1 and 0.5 μM of SAHA alone or with 100 μM TMZ treatment for 72 h. The numbers are relative to control, non-treated cells. i Quantification of oncospheres formed after 7-day treatment with SAHA (0.5 µM) and combined SAHA+TMZ (50 µM) in U87 cells. The numbers are relative to control, non-treated cells (n = 3). j Quantification of P-H3+ cells in untreated, SAHA (0.5 µM), and combined SAHA (0.5 µM) +TMZ (100 µM)-treated GNS166 cells (n = 3)
