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Fig. 1 | BMC Cancer

Fig. 1

From: KRAS is a molecular determinant of platinum responsiveness in glioblastoma

Fig. 1

Sensitivity to cisplatin and resistance to MEK-inhibitor in glioblastoma cells. Panel A—Immunoblots showing ERK 1/2, p-ERK, pan-RAS and KRAS4B protein levels in U87MG and U251MG cells treated with cisplatin (CDDP) 16,6 µM or the MEK-inhibitor PD98059 (40 μM) for the indicated times. Western blot analysis of β-actin was performed in the same experiment, as loading control. The corresponding bar graphs show relative expression of proteins normalized to β-actin. Values are expressed as mean ± s.e.m. (n = 3). Differences between treatments were tested for statistical significance using Student’s matched pairs t-test (*P < 0.0001 compared to untreated sample) or Chi Square test (°P < 0.05 comparing the two cell lines). Panel B – Cell viability measured by MTT. Figure shows 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay at increasing doses of cisplatin (3,3 µM; 6,6 µM; 16,6 µM ( in both cultures. Cells were treated with MTT after 48 h from cisplatin (CDDP) administration and cell viability is expressed as percentage on the control (untreated cells). Panel C shows apoptotic cell percentage analysis assayed by TUNEL cytometry. The percentage of was evaluated after treatment with both cisplatin 16,6 µM or/and the MEK-inhibitor PD98059 (40 μM). Values are expressed as mean ± s.e.m. Differences between treatments were tested for statistical significance using Student’s matched pairs t-test (*P < 0.0001 compared to untreated sample) or Chi Square test (°P < 0.05 comparing the two cell lines)

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