ArticlePloS one2012
Metabolic regulation of invadopodia and invasion by acetyl-CoA carboxylase 1 and de novo lipogenesis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- De novo lipogenesis is essential for platelet production in humans.Nature metabolism · 2020Trial
- Lysosomal lipid metabolism promotes tumor cell invasion through local energetics and membrane lipid remodeling.bioRxiv : the preprint server for biology · 2026Article
- Deleting ACC1 in platelets alters phospholipidome and reduces platelet activation and thrombosis in mice.Blood advances · 2025Article
- Review
- Paired related homeobox 1 attenuates autophagy via acetyl-CoA carboxylase 1-regulated fatty acid metabolism in salivary adenoid cystic carcinoma.FEBS open bio · 2022Article
- Crosstalk between fatty acid metabolism and tumour-associated macrophages in cancer progression.BioMedicine · 2022Review
- Genetic ablation of FASN attenuates the invasive potential of prostate cancer driven by Pten loss.The Journal of pathology · 2021Article
- A novel metabolic function of Myc in regulation of fatty acid synthesis in prostate cancer.Oncogene · 2021Article
- Lipids in the tumor microenvironment: From cancer progression to treatment.Progress in lipid research · 2020Review
- Lipids and cancer: Emerging roles in pathogenesis, diagnosis and therapeutic intervention.Advanced drug delivery reviews · 2020Review
- GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells.International journal of molecular sciences · 2019Article
- Review
- Collagen density modulates triple-negative breast cancer cell metabolism through adhesion-mediated contractility.Scientific reports · 2018Article
- Acetyl-CoA carboxylase 1 regulates endothelial cell migration by shifting the phospholipid composition.Journal of lipid research · 2018Article
- Targeting de novo lipogenesis as a novel approach in anti-cancer therapy.British journal of cancer · 2018Article
- Fatty Acid Synthesis Intermediates Represent Novel Noninvasive Biomarkers of Prostate Cancer Chemoprevention by Phenethyl Isothiocyanate.Cancer prevention research (Philadelphia, Pa.) · 2017Article
- Tristetraprolin disables prostate cancer maintenance by impairing proliferation and metabolic function.Oncotarget · 2016Article
- Fatty Acids and Breast Cancer: Make Them on Site or Have Them Delivered.Journal of cellular physiology · 2016Review
- Identification of AMPK Phosphorylation Sites Reveals a Network of Proteins Involved in Cell Invasion and Facilitates Large-Scale Substrate Prediction.Cell metabolism · 2015Article
- miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene.Carcinogenesis · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Invadopodia are membrane protrusions that facilitate matrix degradation and cellular invasion. Although lipids have been implicated in several aspects of invadopodia formation, the contributions of de novo fatty acid synthesis and lipogenesis have not been defined. Inhibition of acetyl-CoA carboxylase 1 (ACC1), the committed step of fatty acid synthesis, reduced invadopodia formation in Src-transformed 3T3 (3T3-Src) cells, and also decreased the ability to degrade gelatin. Inhibition of fatty acid synthesis through AMP-activated kinase (AMPK) activation and ACC phosphorylation also decreased invadopodia incidence. The addition of exogenous 16∶0 and 18∶1 fatty acid, products of de novo fatty acid synthesis, restored invadopodia and gelatin degradation to cells with decreased ACC1 activity. Pharmacological inhibition of ACC also altered the phospholipid profile of 3T3-Src cells, with the majority of changes occurring in the phosphatidylcholine (PC) species. Exogenous supplementation with the most abundant PC species, 34∶1 PC, restored invadopodia incidence, the ability to degrade gelatin and the ability to invade through matrigel to cells deficient in ACC1 activity. On the other hand, 30∶0 PC did not restore invadopodia and 36∶2 PC only restored invadopodia incidence and gelatin degradation, but not cellular invasion through matrigel. Pharmacological inhibition of ACC also reduced the ability of MDA-MB-231 breast, Snb19 glioblastoma, and PC-3 prostate cancer cells to invade through matrigel. Invasion of PC-3 cells through matrigel was also restored by 34∶1 PC supplementation. Collectively, the data elucidate the novel metabolic regulation of invadopodia and the invasive process by de novo fatty acid synthesis and lipogenesis.
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Registered trials
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.