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G-Protein-Coupled Receptor 120 Mediates DHA-Induced Apoptosis by Regulating IP3R, ROS and, ER Stress Levels in
Jong-Il Shin1, Yong-Joon Jeon1, Sol Lee1
1Department of Biological Sciences, Konkuk University, Seoul 05029, Korea.
Molecules and Cells
|February 16, 2019
Summary
Docosahexaenoic acid (DHA) triggers cancer cell death in drug-resistant gastric cancer by increasing reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress. Targeting G-protein-coupled receptor 120 (GPR120) enhances DHA
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Docosahexaenoic acid (DHA), an omega-3 fatty acid, induces apoptosis and cell cycle arrest in various cancers through reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress.
- The specific mechanisms by which DHA affects drug-resistant cancer cells remain largely unexplored.
Purpose of the Study:
- To investigate the effects of DHA on cisplatin-resistant gastric cancer cells (SNU-601/cis2).
- To elucidate the molecular pathways, including ROS, ER stress, and specific receptors, involved in DHA-induced apoptosis in these resistant cells.
Main Methods:
- Treatment of SNU-601/cis2 cells with DHA.
- Assessment of ROS production, apoptosis, and ER stress markers.
- Utilized inositol 1,4,5-triphosphate receptor (IP3R) blocker (2-APB), G-protein-coupled receptor 120 (GPR120) knockdown via shRNA, and C/EBP homologous protein (CHOP) knockdown.
- ROS scavenger N-acetyl-L-cysteine (NAC) was used for comparison.
Main Results:
- DHA induced ROS-dependent apoptosis in cisplatin-resistant gastric cancer cells.
- Inhibition of IP3R with 2-APB reduced DHA-induced ROS and apoptosis.
- GPR120 expression was confirmed, and its knockdown attenuated DHA-mediated ROS production and apoptosis.
- GPR120 knockdown decreased ER stress response gene expression, similar to NAC or 2-APB treatment.
- CHOP knockdown significantly reduced DHA-mediated apoptosis, highlighting its essential role.
Conclusions:
- GPR120 mediates DHA-induced apoptosis in cisplatin-resistant gastric cancer cells by regulating IP3R, ROS, and ER stress.
- GPR120 represents a potential therapeutic target for overcoming cisplatin resistance in gastric cancer.
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