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. 2020 Jan 22;9:1530. doi: 10.3389/fonc.2019.01530

Figure 4.

Figure 4

MM cells lack full ability to respond by canonical UPR prosurvival signaling after disturbance of ER homeostasis. MM, PC-3 and PFF cells were treated with TG (5 nM), and activation of UPR was analyzed in a time course of 3–24 h. (A) Proteins specific to the three main branches of UPR (i.e., upregulation of GRP78 and IRE1α, and PERK phosphorylation) were detected by Western blot. The data represents at least three repeated experiments. The red square indicates significant upregulation of protein or phosphorylation-induced mobility shift (p-shift; PERK). Numbers indicate mean upregulation as determined by densitometry of chemoluminescence signals of two experiments. (B) Moreover, real-time PCR analysis was performed to monitor changes in HSPA5 (GRP78) and ERN1 (IRE1α) gene expression after BTZ-treatment. Mean ± SD of three independent experiments. (C) Splicing of the XBP1 primary transcript was analyzed in MM and solid tumor cell lines after induction of ER stress. Mean ± SD of three independent experiments. *p < 0.05.