ArticleJournal of cellular and molecular medicine2018
Upregulation of AMPK by 4-O-methylascochlorin promotes autophagy via the HIF-1α expression.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Unlocking the dual role of autophagy: A new strategy for treating lung cancer.Journal of pharmaceutical analysis · 2025Review
- 4-O-Methylascochlorin Synergistically Enhances 5-Fluorouracil-Induced Apoptosis by Inhibiting the Wnt/β-Catenin Signaling Pathway in Colorectal Cancer Cells.International journal of molecular sciences · 2024Article
- 4-O-Methylascochlorin-Mediated BNIP-3 Expression Controls the Balance of Apoptosis and Autophagy in Cervical Carcinoma Cells.International journal of molecular sciences · 2022Article
- Mitofusin-2 boosts innate immunity through the maintenance of aerobic glycolysis and activation of xenophagy in mice.Communications biology · 2021Article
- Protective impact ofToxicology research · 2021Article
- Deoxypodophyllotoxin Inhibits Non-Small Cell Lung Cancer Cell Growth by Reducing HIF-1α-Mediated Glycolysis.Frontiers in oncology · 2021Article
- BNIP3 in Lung Cancer: To Kill or Rescue?Cancers · 2020Review
- Activation of AMPK under Hypoxia: Many Roads Leading to Rome.International journal of molecular sciences · 2020Review
- Alpha7 Nicotinic Acetylcholine Receptor Alleviates Inflammatory Bowel Disease Through Induction of AMPK-mTOR-p70S6K-Mediated Autophagy.Inflammation · 2019Article
- Upregulation of AMPK by 4-O-methylascochlorin promotes autophagy via the HIF-1α expression.Journal of cellular and molecular medicine · 2018Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
4-O-methylascochlorin (MAC) is a derivative of ascochlorin, a prenyl-phenol compound antibiotic isolated from the fungus Ascochyta viciae. MAC induces caspase/poly (ADP-ribose) polymerase-mediated apoptosis in leukemia cells. However, the effects of MAC on autophagy in cancer cells and the underlying molecular mechanisms remain unknown. Here, we show that MAC induces autophagy in lung cancer cells. MAC significantly induced the expression of autophagy marker proteins including LC3-II, Beclin1, and ATG7. MAC promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and its downstream signalling proteins P70S6K and 4EBP1. The AMPK activator AICAR upregulated LC3-II expression through the AMPK/mTOR pathway similar to the effects of MAC. MAC-induced LC3-II protein expression was slightly reduced in AMPK siRNA transfected cells. MAC upregulated hypoxia-inducible factor-1α (HIF-1α) and BNIP3, which are HIF-1α-dependent autophagic proteins. Treatment with CoCl
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.