ArticleInternational journal of oncology2017
AICAR induces mitochondrial apoptosis in human osteosarcoma cells through an AMPK-dependent pathway.
Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Single-cell and multi-omics integrative modeling identifies mitochondrial gene HSPE1 as a therapeutic target in osteosarcoma.Journal of translational medicine · 2026Article
- Nanomaterial-induced mitochondrial biogenesis enhances intercellular mitochondrial transfer efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PHGDH inhibition and FOXO3 modulation drives PUMA-dependent apoptosis in osteosarcoma.Cell death & disease · 2025Article
- The Role of Adenosine in Overcoming Resistance in Sarcomas.International journal of molecular sciences · 2024Review
- Article
- The role of AMPK in cancer metabolism and its impact on the immunomodulation of the tumor microenvironment.Frontiers in immunology · 2023Review
- Multi-omics analysis reveals cuproptosis and mitochondria-based signature for assessing prognosis and immune landscape in osteosarcoma.Frontiers in immunology · 2023Article
- Mitochondria-Targeted, Nanoparticle-Based Drug-Delivery Systems: Therapeutics for Mitochondrial Disorders.Life (Basel, Switzerland) · 2022Review
- A mitochondria-related signature for predicting immune microenvironment and therapeutic response in osteosarcoma.Frontiers in oncology · 2022Article
- Insulin and 5-Aminoimidazole-4-Carboxamide Ribonucleotide (AICAR) Differentially Regulate the Skeletal Muscle Cell Secretome.Proteomes · 2021Article
- PF-06409577 Activates AMPK Signaling and Inhibits Osteosarcoma Cell Growth.Frontiers in oncology · 2021Article
- Triple negative breast cancer: special histological types and emerging therapeutic methods.Cancer biology & medicine · 2020Review
- Pioglitazone and Deoxyribonucleoside Combination Treatment Increases Mitochondrial Respiratory Capacity in m.3243A>G MELAS Cybrid Cells.International journal of molecular sciences · 2020Article
- Mitochondrial Dysfunction in the Transition from NASH to HCC.Metabolites · 2019Review
- AMP-activated protein kinase: a potential therapeutic target for triple-negative breast cancer.Breast cancer research : BCR · 2019Review
- The AMPK-activator AICAR in thyroid cancer: effects on CXCL8 secretion and on CXCL8-induced neoplastic cell migration.Journal of endocrinological investigation · 2018Article
- HuR stabilizes TFAM mRNA in an ATM/p38-dependent manner in ionizing irradiated cancer cells.Cancer science · 2018Article
- Anticancer effects of resveratrol in canine hemangiosarcoma cell lines.Veterinary and comparative oncology · 2018Article
- Polyphyllin II (PPII) Enhances the Sensitivity of Multidrug-resistant A549/DDP Cells to Cisplatin by Modulating Mitochondrial Energy Metabolism.In vivo (Athens, Greece)Article
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12 authors.
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Abstract
The AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) modulates cellular energy metabolism, and promotes mitochondrial proliferation and apoptosis. Previous studies have shown that AICAR has anticancer effects in various cancers, however the roles of AMPK and/or the effects of AICAR on osteosarcoma have not been reported. In the present study, we evaluated the effects of AICAR on tumor growth and mitochondrial apoptosis in human osteosarcoma both in vitro and in vivo. For in vitro experiments, two human osteosarcoma cell lines, MG63 and KHOS, were treated with AICAR, and the effects of AICAR on cell growth and mitochondrial apoptosis were assessed by WST assays, TUNEL staining, and immunoblot analyses. In vivo, human osteosarcoma-bearing mice were treated with AICAR, and the mitochondrial proliferation and apoptotic activity in treated tumors were assessed. In vitro experiments revealed that AICAR activated AMPK, inhibited cell growth, and induced mitochondrial apoptosis in both osteosarcoma cell lines. In vivo, AICAR significantly reduced osteosarcoma growth without apparent body weight loss and AICAR increased both mitochondrial proliferation and apoptotic activity in treated tumor tissues. AICAR showed anticancer effects in osteosarcoma cells through an AMPK-dependent peroxisome proliferator‑activated receptor-γ coactivator-1α (PGC-1α)/mitochondrial transcription factor A (TFAM)/mitochondrial pathway. The findings in this study strongly suggest that AICAR could be considered as a potent therapeutic agent for the treatment of human osteosarcoma.
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