Fig. 5: CAV1 mediated inhibition of UPR in tumors requires serine-80.

B16F10(Mock), B16F10(CAV1) or B16F10(CAV1/S80A) cells were grown in the presence of IPTG (1 mM) for 48 h to induce CAV1 expression. Then, cells (300,000) were injected subcutaneously into C57BL/6 mice and tumor progression was evaluated up to 15 days when mice were sacrificed. a Tumor volumes for each group (n = 3, mean ± SEM) were monitored every three days and are shown from day 1 to 15. b Tumor volume measured for each group obtained at day 15 (n = 7, mean ± SEM, Kruskal–Wallis test, **p = 0.0018, *p < 0.05). c At day 15, tumors from each group were processed, total RNA was extracted and Xbp1 mRNA splicing was detected and quantified by scanning densitometry. Results are expressed as the percentage of splicing (s/s + u) × 100 (s: spliced, u: unspliced; n = 5 Mock, n = 13 CAV1, n = 7 CAV1/S80A, mean ± SEM, Kruskal–Wallis test, **p = 0.0023). d The mRNA levels of the IRE1α target genes Sec61 and Wsf1 were evaluated by qPCR. All values were standardized to β-actin used as an internal control (n = 4, mean ± SEM, Kruskal–Wallis test, *p < 0.05). e Two target genes of the PERK pathway, Chop and Bip were evaluated by qPCR. All values were standardized to β-actin used as an internal control (n = 4, mean ± SEM, Kruskal–Wallis test, *p < 0.05).