Cellular signalling · 2025
GCN2 promotes fatty acid metabolism through the activation of PI3K/AKT signaling in gastric cancer.
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Sun Dong, Sun Xu, Wang Xiaofeng, Zhang Jiazi, Liu Liqing, Xie Jiaping
Аннотация
PURPOSE: Our purpose was to investigate the impact and molecular mechanisms of GCN2 on gastric cancer.
METHODS: GCN2 expressions were measured in gastric cancer cells and tissues via qRT-PCR, western blot and immunohistochemistry staining. Cell functional assays were performed to elucidate the role of GCN2 in cell proliferation, apoptosis, migration, and invasion. BODIPY 493/503 staining was employed to assess the change of lipid droplets induced by GCN2. Additionally, the proteins expression was examined by western blot. Additionally, mice tumor xenograft models were also developed for in vivo analysis.
RESULTS: GCN2 was overexpressed in gastric cancer. GCN2 facilitated malignant behaviors of gastric cancer cells. Furthermore, GCN2 was found to facilitate the fatty acid metabolism in gastric cancer cells. Moreover, PI3K/Akt/mTOR signaling was activated by GCN2. Besides, rescue experiments results manifested that 740YP could attenuated the impact of GCN2 on the malignant behaviors and fatty acid metabolism of gastric cancer cells. Xenograft tumor models further demonstrated that GCN2 knockdown inhibited the growth of gastric cancer tumors by suppressing PI3K/AKT/mTOR signaling pathway.
CONCLUSION: This study provided evidences that GCN2 could promote fatty acid metabolism and tumor progression through the activation of PI3K/AKT/mTOR signaling in gastric cancer.
METHODS: GCN2 expressions were measured in gastric cancer cells and tissues via qRT-PCR, western blot and immunohistochemistry staining. Cell functional assays were performed to elucidate the role of GCN2 in cell proliferation, apoptosis, migration, and invasion. BODIPY 493/503 staining was employed to assess the change of lipid droplets induced by GCN2. Additionally, the proteins expression was examined by western blot. Additionally, mice tumor xenograft models were also developed for in vivo analysis.
RESULTS: GCN2 was overexpressed in gastric cancer. GCN2 facilitated malignant behaviors of gastric cancer cells. Furthermore, GCN2 was found to facilitate the fatty acid metabolism in gastric cancer cells. Moreover, PI3K/Akt/mTOR signaling was activated by GCN2. Besides, rescue experiments results manifested that 740YP could attenuated the impact of GCN2 on the malignant behaviors and fatty acid metabolism of gastric cancer cells. Xenograft tumor models further demonstrated that GCN2 knockdown inhibited the growth of gastric cancer tumors by suppressing PI3K/AKT/mTOR signaling pathway.
CONCLUSION: This study provided evidences that GCN2 could promote fatty acid metabolism and tumor progression through the activation of PI3K/AKT/mTOR signaling in gastric cancer.
Предметные рубрики MeSH
Stomach NeoplasmsHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnimalsSignal TransductionFatty AcidsCell Line, TumorCell ProliferationMiceProtein Serine-Threonine KinasesMice, NudeApoptosisMice, Inbred BALB CTOR Serine-Threonine KinasesCell MovementMaleFemaleGene Expression Regulation, Neoplastic