Fig. 1: Osimertinib treatment inhibits GBM cell proliferation and induces cell cycle arrest.
From: Osimertinib induces paraptosis and TRIP13 confers resistance in glioblastoma cells

A GBM cell lines (LN-18, LN-229, SF-539, and U87MG) were vehicle-treated or treated with varying concentrations of Osimertinib (2.5, 5, and 10 μM) for 24, 48, 72 h. Cell growth inhibition was determined using a CCK8 assay. B GBM Cells (LN-18, LN-229, SF-539, and U87MG) were treated with vehicle or 5 μm Osimertiinb, then cultured in a complete medium for 12 days for colony formation analysis. Results represent as the mean ± SD, n = 6, **p < 0.01. C GBM cells were pre-treated as in B for 24 h and seeded in ultra-low attachment 96-well plates for 7 days. Scale bar = 100 μm. D LN-229 and U87MG cells were treated the same as in A and were analyzed by FACS after staining with propidium iodide for cell cycle analysis at 24 h. Results represent the mean ± SD, *p < 0.05, **p < 0.01. E LN-229 and U87MG cells were treated the same as in A, and protein levels of CyclinD1 and GAPDH were analyzed by immunoblot analysis (IB). F Time course analysis of levels of CyclinD1 and GAPDH by IB in LN-229 and U87MG cells treated the same as in B. G LN-229 and U87MG cells were treated the same as in D, protein levels of P-AKT(S473), AKT, P-ERK1/2, ERK1/2 and GAPDH were analyzed by IB. H Mice’s brain-bearing LN-229 or U87MG xenografts were vehicle-treated or treated with Osimertinib (50 mg/kg) for 2 weeks. Representative images of H&E-stained brain tumor xenografts were shown (H). Tumor volume is represented as the mean ± SD, n = 7, ****p < 0.0001. Data represent three independent experiments with similar results. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.