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Fig. 1 | Molecular Cancer

Fig. 1

From: Shedding of bevacizumab in tumour cells-derived extracellular vesicles as a new therapeutic escape mechanism in glioblastoma

Fig. 1

IgG1/Bevacizumab antibody can affect LN18 and U87 GBM cells-derived EVs concentration and their proteomic content. NTA of a LN18 or b U87 GBM cells-derived EVs following treatment with bevacizumab (0.25 mg/mL). LN18 or U87 GBM cells were treated for 24 h with 0.25 mg/mL IgG1 or bevacizumab. Then cells were washed two times with sterile PBS and incubated additional 24 h in serum free conditions without treatment. CM was then collected, EVs were isolated and re-suspended in 100 μL filtered sterile PBS. EVs suspension was 1/5 diluted and infused to a Nanosight© NS300 instrument. 5 captures of 60s each were recorded. Particles concentration (particles/mL) and size (nm) were measured. Particles concentration was normalised to the number of cells after treatment (particles/mL/cell). The mean ± SEM of 3 independent experiments is shown. c Western blotting validation of the human IgG, Annexin A2 and CD44 in EVs derived from LN18 and U87 GBM cells. d Gene expression distribution of Annexin A2 and CD44 among the different GBM subtypes has been obtained from TCGA. The mean ± SEM is shown (*p < 0.05, **p < 0.01, ***p < 0.001,****p < 0.0001; ANOVA, compare to ‘normal’)

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