ArticleFrontiers in oncology2022
Metformin-induced AMPK activation promotes cisplatin resistance through PINK1/Parkin dependent mitophagy in gastric cancer.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Autophagy as a therapeutic target for cisplatin-resistant gastric cancer.Genes & diseases · 2026Review
- Article
- Mitophagy interacts with mitochondrial dynamics and biogenesis, acting as a double-edged sword in digestive cancer.iScience · 2026Review
- New Functions of Mitochondrial Dysfunction in Gastric Cancer: From Molecular Processes to Potential Treatments.International journal of molecular sciences · 2026Review
- Knocking down CLDN7 enhanced the effect of cisplatin in OC cells by regulating mitophagy.Journal of ovarian research · 2026Article
- Mitochondrial Dysfunction as a Targetable Vulnerability in Gastric Cancer: From Carcinogenesis to Apoptosis (A Narrative Review).Journal of Cancer · 2026Review
- Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance.Translational oncology · 2025Article
- Study on the regulation of gastric cancer cell apoptosis by LACTB through mitochondrial autophagy pathway.Scientific reports · 2025Article
- Pleiotropic Effects of Metformin on the Chemotherapy Response of HPV-Positive Cancer Cells.Journal of medical virology · 2025Article
- DAZAP1 maintains gastric cancer stemness by inducing mitophagy.JCI insight · 2025Article
- Metformin Enhances the Chemosensitivity of Gastric Cancer to Cisplatin by Downregulating Nrf2 Level.Analytical cellular pathology (Amsterdam) · 2025Article
- Utilizing Multi-omics analysis to elucidate the role of mitochondrial gene defects in Gastric cancer progression.PloS one · 2025Article
- Receptor-Interacting Protein Kinase 3-Mediated Modulation of Endothelial Cell Necroptosis and Mitochondrial Dysfunction through AMPK/Drp1 Signaling Pathway: Insights into the Pathophysiological Mechanisms of Lipopolysaccharide-Induced Acute Lung Injury.International journal of medical sciences · 2025Article
- Ginsenoside RG3 Synergizes With STING Agonist to Reverse Cisplatin Resistance in Gastric Cancer.Food science & nutrition · 2025Article
- The Role of Adenosine in Overcoming Resistance in Sarcomas.International journal of molecular sciences · 2024Review
- Sesamol-mediated targeting of EPHA2 sensitises cervical cancer for cisplatin treatment by regulating mitochondrial dynamics, autophagy, and mitophagy.Molecular biology reports · 2024Article
- FoxG1/BNIP3 axis promotes mitophagy and blunts cisplatin resistance in osteosarcoma.Cancer science · 2024Article
- From macroautophagy to mitophagy: Unveiling the hidden role of mitophagy in gastrointestinal disorders.World journal of gastroenterology · 2024Article
- p32/OPA1 axis-mediated mitochondrial dynamics contributes to cisplatin resistance in non-small cell lung cancer.Acta biochimica et biophysica Sinica · 2024Article
- Targeting mitophagy for neurological disorders treatment: advances in drugs and non-drug approaches.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is one of the most common tumors worldwide, and cisplatin is a standard chemotherapeutic reagent for GC treatment. However, chemoresistance is an inherent challenge which limits its application and effectiveness in clinic. This study aims to investigate the mechanism of metformin-induced cisplatin resistance in GC. Intriguingly, the upregulation of mitophagy markers, mitochondrial fission, autophagy and mitophagosome were observed in SGC-7901/DDP cells compared to those in the SGC-7901 cells. Treatment with metformin significantly increased mitochondrial fission and mitophagy in both AGS and SGC-7901 cells, resulting in decreased ATP production, which unexpectedly protected GC cells against the cytotoxicity of cisplatin. In contrast, application of Chloroquine and 3-methyladenine, two inhibitors of autophagy, significantly alleviated the protective effect of metformin on SGC-7901 and AGS cells against cytotoxicity of cisplatin. Moreover, metformin also stimulated the phosphorylation of AMPK (Thr172) and increased the expression of mitophagy markers including Parkin and PINK1 in the AMPK signaling-dependent manner. Consistently, the cell viability and cell apoptosis assay showed that metformin-induced cisplatin resistance was prevented by knockdown of AMPKα1. Taken together, all data in this study indicate that metformin induced AMPK activation and PINK1/Parkin dependent mitophagy, which may contribute to the progression of cisplatin resistance in GC.
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