Fig. 2: Sunitinib activates ER stress response in ccRCC cells. | Cell Death & Disease

Fig. 2: Sunitinib activates ER stress response in ccRCC cells.

From: The convergent roles of NF-κB and ER stress in sunitinib-mediated expression of pro-tumorigenic cytokines and refractory phenotype in renal cell carcinoma

Fig. 2

a Time-course of sunitinib-induced ER stress and NF-κB activation. 786-O ccRCC cells were treated with 10 μM of sunitinib for the indicated periods of time. Total cell lysates were subjected to western blot analysis using specific antibodies. b Treatment with sunitinib does not affect IRE1α-mediated Xbp1 splicing under ER stress conditions. 786-O cells were pre-treated with 5 μM of the PERK inhibitor GSK2656157 (PERKi) or 1 μM of the IRE1α inhibitor 4μ8c for 1 h followed by incubation in the presence or absence of sunitinib (10 μM) (Sun) or thapsigargin (1 μM) (TG) for 4 h. To explore whether treatment with sunitinib affects Xbp1 splicing under ER stress, 786-O cells were pre-incubated with sunitinib (10 μM) for 1 h followed by treatment with thapsigargin (1 μM) for 4 h. Total RNA was subjected to RT-PCR with specific primers spanning Xbp1 cleavage site. RT-PCR products were then separated in 2.5% agarose gel to detect spliced (lower band, 311 bp) and unspliced (upper band, 337 bp) fragments

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