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. 2017 Sep 21;8(58):98298–98311. doi: 10.18632/oncotarget.21176

Figure 5. COMP protects cancer cells against apoptosis.

Figure 5

ER stress-mediated apoptosis was induced in the transfected cells with Brefeldin A. Cells expressing COMP were less apoptotic as compared to mock (A). Similar results were obtained when apoptosis was induced via the TNFR1 pathway (B). Apoptosis was, then, induced by inhibiting protein translation (CHX, cycloheximide), RNA synthesis (actinomycin D), protein kinases (staurosporine) or nuclear topoisomerase (camptothecin and etoposide). COMP expression was protective against all apoptotic stimuli except inhibition of nuclear topoisomerase (C). Furthermore, COMP expression protected the cells against apoptosis induced by Docetaxel (D). Addition of recombinant COMP to mock-trasfected cells could not protects the cells against apoptosis induced by staurosporin, suggesting that the protective effect is mediated by intracellular COMP (E). The data represent at least three independent experiments ±SD and was compared to mock by 2-way ANOVA with Bonferroni post-test (A-D), or compared to BSA by 1-way ANOVA with Dunnett's multiple comparison test (E), ns, not significant; *, p < 0.05; **, p < 0.005; ***, p < 0.001.