Fig. 1: Effects of TMZ and perifosine as monotherapies and a combination therapy on the viability and proliferation of glioblastoma cells. | Cell Death Discovery

Fig. 1: Effects of TMZ and perifosine as monotherapies and a combination therapy on the viability and proliferation of glioblastoma cells.

From: The combination of temozolomide and perifosine synergistically inhibit glioblastoma by impeding DNA repair and inducing apoptosis

Fig. 1

A Prognostic analysis of the four groups: non-TMZ-treated + high AKT1 expression, non-TMZ-treated + low AKT1 expression, TMZ-treated + high ATK1 expression, and TMZ-treated + low AKT1 expression. B DEGs between the TMZ-treated + high ATK1 expression and TMZ-treated + low AKT1 expression groups. C KEGG pathway analysis suggested that apoptosis is the main form of cell death. D U87MG and U251 cells were treated with TMZ alone, perifosine (PRF) alone, or TMZ and perifosine in combination for 48 h. The cells were then observed under an inverted microscope. Scale bar: 100 μM. E, F U87MG and U251 cell viability was determined using a CCK-8 assay after treatment with TMZ (0, 50, 100, 150 μM) alone, perifosine (0, 2.5, 5, 10 μM) alone or TMZ and perifosine in combination for 48 h. G, H 3D synergy plot of U87MG and U251 cells treated with TMZ alone or in combination with each of the other drugs. The red areas represent synergistic combinations (those with a synergy score of greater than 10). ZIP synergy scores were calculated using the SynergyFinder web application (version 3.0). I Colony formation assays were performed to verify the effect of the combination of TMZ and perifosine on glioblastoma cell proliferation. **p < 0.01, ***p < 0.001, and ****p < 0.0001 based on one-way ANOVA followed by Dunnett’s test for multiple comparisons.

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