ArticleCell death & disease2016
Phospholipase D1-regulated autophagy supplies free fatty acids to counter nutrient stress in cancer cells.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- HSD17B7 Counters Bone Loss in Estrogen Deficiency via Estrogen Receptor Stabilization and Mediates the Effect of Raloxifene.MedComm · 2026Article
- Phospholipase D: emerging therapeutic targets in signaling, metabolism, and immune-oncology.Cell communication and signaling : CCS · 2025Review
- Article
- Adaptation mechanisms in cancer: Lipid metabolism under hypoxia and nutrient deprivation as a target for novel therapeutic strategies (Review).Molecular medicine reports · 2025Review
- PLD1 promotes spindle assembly and migration through regulating autophagy in mouse oocyte meiosis.Autophagy · 2024Article
- Identification of a lipid homeostasis-related gene signature for predicting prognosis, immunity, and chemotherapeutic effect in patients with gastric cancer.Scientific reports · 2024Article
- A metabolomic and proteomic study to elucidate the molecular mechanisms of immunotherapy resistance in patients with oesophageal squamous cell carcinoma.Biomedical reports · 2023Article
- The crosstalk among the physical tumor microenvironment and the effects of glucose deprivation on tumors in the past decade.Frontiers in cell and developmental biology · 2023Review
- Article
- Nanog mediated by FAO/ACLY signaling induces cellular dormancy in colorectal cancer cells.Cell death & disease · 2022Article
- Ameliorating cancer cachexia by inhibiting cancer cell release of Hsp70 and Hsp90 with omeprazole.Journal of cachexia, sarcopenia and muscle · 2022Article
- PLD1 promotes reactive oxygen species production in vascular smooth muscle cells and injury-induced neointima formation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022Article
- Phosphatidylcholine-Derived Lipid Mediators: The Crosstalk Between Cancer Cells and Immune Cells.Frontiers in immunology · 2022Review
- Exploration of Lipid Metabolism in Gastric Cancer: A Novel Prognostic Genes Expression Profile.Frontiers in oncology · 2021Article
- Mammalian phospholipase D: Function, and therapeutics.Progress in lipid research · 2020Review
- Metabolic Reprogramming in CD8Frontiers in immunology · 2020Review
- Emerging roles of ATG proteins and membrane lipids in autophagosome formation.Cell discovery · 2020Review
- Mitochondria-centric bioenergetic characteristics in cancer stem-like cells.Archives of pharmacal research · 2019Review
- Proliferative and metastatic roles for Phospholipase D in mouse models of cancer.Advances in biological regulation · 2018Review
- Binding of PLD2-Generated Phosphatidic Acid to KIF5B Promotes MT1-MMP Surface Trafficking and Lung Metastasis of Mouse Breast Cancer Cells.Developmental cell · 2017Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Cancer cells utilize flexible metabolic programs to maintain viability and proliferation under stress conditions including nutrient deprivation. Here we report that phospholipase D1 (PLD1) participates in the regulation of metabolic plasticity in cancer cells. PLD1 activity is required for cancer cell survival during prolonged glucose deprivation. Blocking PLD1 sensitizes cancer cells to glycolysis inhibition by 2-deoxy-D-glucose (2-DG) and results in decreased autophagic flux, enlarged lysosomes, and increased lysosomal pH. Mechanistically, PLD1-regulated autophagy hydrolyzes bulk membrane phospholipids to supply fatty acids (FAs) for oxidation in mitochondria. In low glucose cultures, the blockade of fatty acid oxidation (FAO) by PLD1 inhibition suppresses adenosine triphosphate (ATP) production and increases reactive oxygen species (ROS), leading to cancer cell death. In summary, our findings reveal a novel role of PLD1 in sustaining cancer cell survival during metabolic stress, and suggest PLD1 as a potential target for anticancer metabolism therapy.
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