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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: Protein disulfide-isomerase A4 confers glioblastoma angiogenesis promotion capacity and resistance to anti-angiogenic therapy

Fig. 7

Mechanism diagram of XBP1/PDIA4/VEGFA axis in GBM. Under the extracellular stress, ER stress of GBM cell would start, and activates the unfolded protein pathway (URP), which will upregulate the X-box binding protein 1 (XBP1), and then transcriptionally upregulated PDIA4 expression. As an ER stress effect protein, PDIA4 could increase the expression and secretion of VEGFA protein in GBM cells, and activate the tumor associated endothelial cell. This mechanism elicits the pro-angiogenesis function of PDIA4 of GBM

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