Research Paper Volume 12, Issue 17 pp 17459—17479

Figure 1. Establishment of RCC sunitinib resistant cell lines. (A) Cell viability of resistant cells ACHN-R, 786-O-R and parental cells ACHN, 786-O in sunitinib concentration gradients. (B) Western blotting analysis of c-PARP1and phosphorylated and total STAT3, AKT1 and ERK1/2 after sunitinib treatment in resistant and parental cell lines. β-actin served as the loading control. (C) Transwell assays of resistant and parental cells with/without sunitinib treatment. (D) CCK8 assays of resistant and parental cells with/without sunitinib treatment. (E) Colony formation of resistant and parental cells with/without sunitinib treatment. Each experiment was performed at least three times and data was represented as mean ± SEM. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. RCC, renal cell carcinoma; c-PARP1, cleaved poly(ADP-ribose) polymerase 1; STAT3, signal transducer and activator of transcription 3; AKT1, AKT serine/threonine kinase 1; ERK1/2, mitogen-activated protein kinase 3/1; CCK8, cell counting kit-8.