Fig. 4: Sunitinib-induced expression of IL-6, IL-8 and TNFα depends on activation of PERK branch of ER stress. | Cell Death & Disease

Fig. 4: Sunitinib-induced expression of IL-6, IL-8 and TNFα depends on activation of PERK branch of ER stress.

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. 4

a Induction of ER stress in ccRCC cells results in upregulation of IL-6, IL-8 and TNFα expression. 786-O cells were pre-treated with 5 μM of the PERK inhibitor, GSK2656157 (PERKi) or 1 μM of the IRE1α inhibitor 4μ8 C for 1 h followed by incubation in the presence or absence of sunitinib (10 μM) (Sun) or thapsigargin (1 μM) (TG) for 4 h. Cytokines expression levels were analyzed by qRT-PCR. Data are presented as the mean ± S.D. *P < 0.05; **P < 0,001; ***P < 0.0005 when compared with cells cultured in medium only (Med). b The effects of IKKβ, TRAF2 and PERK knockouts on sunitinib-induced cytokine production in 786-O cells. Wild-type (WT) 786-O cells and their knockout counterparts were treated with 10 μM of sunitinib for 3 h. Cytokines expression levels were analyzed by qRT-PCR. Data are presented as the mean ± S.D. ***P < 0.0005

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