Fig. 6: P-gp is involved in GAL1-mediated resistance to DOX in HepG2 cells. | Cell Death & Disease

Fig. 6: P-gp is involved in GAL1-mediated resistance to DOX in HepG2 cells.

From: Galectin-1 confers resistance to doxorubicin in hepatocellular carcinoma cells through modulation of P-glycoprotein expression

Fig. 6

Cell viability (MTT assay) of GAL1-overexpressing and HepG2-M cells co-incubated with 2 µM DOX and A verapamil (P-gp inhibitor) or C probenecid (MRP2 inhibitor) at the indicated concentrations for 24 h. Results are expressed as the mean of cell viability percentage with respect to the corresponding untreated cell line (100%) ± SEM (n = 4). ns: no significant difference. *p < 0.05 compared with DOX-treatment HepG2-GAL1 cells without verapamil. B Western blot and densitometric analysis showing relative MRP2 expression in GAL1-overexpressing and control HepG2 cells. β-tubulin was used as loading control (n = 4). *p < 0.05 with respect to HepG2-M cells. D Western blot and densitometric analysis showing relative P-gp expression in HepG2-GAL1 cells after transfection with siRNA to specifically knockdown this transporter (HepG2-GAL1-siPgp cells) or with scrambled siRNA as control (HepG2-GAL1-siScr cells). β-tubulin was used as loading control (n = 4). ***p < 0.001 with respect to control cells. E, F Cell viability (MTT assay) in HepG2-GAL1-siScr and HepG2-GAL1-siPgp cells incubated in the absence (control) or the presence of DOX (2 µM) (E) or sorafenib (30 µM) (F) for 24 h. Results are expressed as the mean of cell viability percentage with respect to untreated siRNA scrambled transfected cells (100%) ± SEM (n = 5). *p < 0.05 with respect to DOX-treated HepG2-GAL1-siScr cells. ns: no significant difference.

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