The integrated stress response-associated signals modulates intestinal tumor cell growth by NSAID-activated gene 1 (NAG-1/MIC-1/PTGF-beta)

Carcinogenesis
Hyun YangYuseok Moon

Abstract

Phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) is a critical convergence point of the integrated stress response (ISR), which supports eukaryotic cellular adaptation to diverse stressful conditions, including the endoplasmic reticulum (ER) stress by global protein translational arrest and induction of numerous stress-triggered cytoprotective genes. Challenge with non-steroidal anti-inflammatory drug (NSAID) leads to ER perturbation that may sensitize cancer cells to drug-induced apoptosis. Here, we examined the ER stress signals in the context of NSAID exposure and the induction of the critical tumor suppressor, NSAID-activated gene 1 (NAG-1), in the epithelial cancer cells. Sulindac sulfide, the active sulindac metabolite, was shown to trigger the ISRs via eIF2alpha kinase such as RNA-dependent protein kinase-related endoplasmic reticulum kinase (PERK) and RNA-dependent protein kinase (PKR). ER stress markers such as glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and activating transcription factor (ATF)-3 were enhanced by sulindac sulfide in colon cancer cells. In these cells, the PERK-activated ATF3-CHOP signaling pathway mediated the gene expression of pro-apoptotic NA...Continue Reading

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Feb 21, 2013·Journal of Health Care for the Poor and Underserved·Christopher C WilliamsElena V Skripnikova
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Dec 29, 2020·Biochimica Et Biophysica Acta. General Subjects·Kook Hwan Kim, Myung-Shik Lee

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