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Salvigenin inhibits gastric cancer progression by suppressing the EGFR/PI3K/AKT pathway
Kuan Qiao1, Zeqi Yang2, Ying Fang3
1Department of Gastroenterology, Yantaishan Hospital, Yantai, Shandong, 264003, China.
Background:
Salvigenin recently been shown to possess antitumor properties. However, no study has focused on the underlying relationship of salvigenin with gastric cancer (GC). This study aimed to explore salvigenin function on GC and delineate the potential molecular mechanisms.
Methods:
The effects of salvigenin on the malignant behavior of GC cells were explored using colony formation, EdU, flow cytometry, scratch as well as transwell assays. The potential mechanisms of action of salvigenin in GC were explored through network pharmacology analysis, molecular docking, Western blot, immunofluorescence staining, and rescue experiments. Besides, the in vivo effects of salvigenin on GC were assessed using a xenograft mouse model.
Results:
Salvigenin could suppress the proliferative, migratory and invasive capabilities of GC cells, while facilitating apoptosis. Furthermore, salvigenin could inactivate EGFR/PI3K/AKT pathway in AGS and HGC-27 cells. Additionally, rescue experiments using NSC 228155 and EGFR overexpression further confirmed that activating EGFR/PI3K/AKT signaling could reverse the effects of salvigenin on the malignant behavior of GC cells. In addition, salvigenin was also confirmed to repress GC tumor growth in vivo via inactivating EGFR/PI3K/AKT signaling.
Conclusion:
Salvigenin might suppress the proliferative, migratory, and invasive capacity, but facilitate the apoptotic ability in GC through inactivating EGFR/PI3K/AKT signaling.
Insights
Salvigenin suppresses gastric cancer (GC) cell proliferation, migration, and invasion while promoting apoptosis. This effect is achieved by inhibiting the epidermal growth factor receptor (EGFR)/phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Salvigenin exhibits antitumor properties, but its role in gastric cancer (GC) remains unexplored.
- Gastric cancer is a significant global health concern requiring novel therapeutic strategies.
Purpose of the Study:
- To investigate the anti-gastric cancer effects of salvigenin.
- To elucidate the molecular mechanisms underlying salvigenin's action in GC.
Main Methods:
- In vitro assays (colony formation, EdU, flow cytometry, scratch, transwell) assessed GC cell behavior.
- Network pharmacology, molecular docking, Western blot, immunofluorescence, and rescue experiments identified molecular targets.
- In vivo xenograft mouse models evaluated salvigenin's efficacy against GC tumors.
Main Results:
- Salvigenin inhibited GC cell proliferation, migration, and invasion while inducing apoptosis.
- Salvigenin inactivated the EGFR/PI3K/AKT signaling pathway in GC cells.
- In vivo studies confirmed salvigenin's repression of GC tumor growth via EGFR/PI3K/AKT pathway inhibition.
Conclusions:
- Salvigenin demonstrates potential as an anti-gastric cancer agent.
- Inhibition of the EGFR/PI3K/AKT pathway is a key mechanism for salvigenin's anti-cancer effects in GC.
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