Skip to main content
Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: SF3B1 inhibition disrupts malignancy and prolongs survival in glioblastoma patients through BCL2L1 splicing and mTOR/ß-catenin pathways imbalances

Fig. 5

Pharmacological inhibition of SF3B1 with pladienolide B in vitro decreases critical functional parameters of aggressiveness and key tumor development/progression/aggressiveness markers in GBM cells compared to control conditions. a Schematic representation of the effect of pladienolide B inhibiting SF3B1. Proliferation rate in response to pladienolide B administration in GBM cell lines (U-87 MG and U-118 MG; n = 5) (b), in primary patient-derived GBM cells (n = 6) (c), and in primary non-tumor brain cell cultures (n = 3) (d). e Migration rate after pladienolide B in U-118 MG cells (representative images of the migration capacity are also included; n = 5). f Tumorsphere formation assay showing sphere area and number of tumorspheres per well in response to pladienolide B administration in U-87 MG and U-118 MG cells (n = 3; representative images of tumorspheres formation are also included). g VEGF secretion in response to pladienolide B in U-87 MG and U-118 MG cells (n = 3). h Apoptosis rate after pladienolide B administration in U-87 MG and U-118 MG cells (n = 3). i Protein levels of cleaved-caspase 3 after 24 h of incubation with pladienolide B determined by western blot (n = 3). j Summary of the effect of pladienolide B treatment on the different functional parameters previously mentioned. Expression of different tumor progression markers after pladienolide B treatment in the two GBM cell lines (k) and in primary patient-derived GBM cells (l). Expression of critical oncogenic spliceosome components after pladienolide B treatment in the two GBM cell lines (m) and in primary patient-derived GBM cells (n). Asterisks (*P < 0.05; **P < 0.01; ***P < 0.001) indicate statistically significant differences across different conditions

Back to article page