Fig. 5: Knockdown of KRT8 followed by chemotherapy promoted apoptosis of chordoma cells through aggregating ER stress through PERK/eIF2α arm of UPR in vitro. | Cell Death & Disease

Fig. 5: Knockdown of KRT8 followed by chemotherapy promoted apoptosis of chordoma cells through aggregating ER stress through PERK/eIF2α arm of UPR in vitro.

From: Knockdown of cytokeratin 8 overcomes chemoresistance of chordoma cells by aggravating endoplasmic reticulum stress through PERK/eIF2α arm of unfolded protein response and blocking autophagy

Fig. 5

Chordoma cell line CM319 and UCH1 were transfected with siKRT8 followed by treatment of doxorubicin (0.5 μM) or irinotecan (50 μM) for 24 h. a Splicing of XBP1 mRNA were evaluated by qRT-PCR. b Western blotting analysis and quantification of PERK, p-PERK, eIF2α, p-eIF2α, ATF6, and XBP1-s protein expression (p-PERK and p-eIF2α were normalized to PERK and eIF2α expression, respectively; ATF6 and XBP1-s were normalized to GAPDH expression; quantification data of ATF6 in “Doxo 24 h” group and “Irino 24 h” group was derived from the same data set in Fig. 2b) (n = 3, *p < 0.05 vs. indicated group, **p < 0.01 vs. indicated group, NS: not statistically significant vs. indicated group, Con: control group, Doxo: doxorubicin-treated group, Irino: irinotecan-treated group. For all the above-mentioned statistical analyses, significance was determined by one-way ANOVA followed by Tukey’s multiple comparisons test and the results were shown as mean ± SD).

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