Abstract
Endoplasmic Reticulum (ER) is an important site for protein folding and maturation. Accumulation of unfolded or misfolded proteins in the ER leads to “ER stress”. The unfolded protein response (UPR) is a finely regulated cell-signaling program to re-establish ER folding capacity for building up cellular homeostasis. Although ER stress modulators have emerged as promising treatment options with their potential to trigger ER stress-mediated apoptosis in cancer cells, here we show that ER stress upregulates VEGF (Vascular Endothelial Growth Factor) expression and secretion in colon cancer cells, which may result in resistance against the treatment through enhanced autocrine/intracrine VEGF signaling and through supporting further angiogenesis.
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