ArticleNature communications2019
EGFL9 promotes breast cancer metastasis by inducing cMET activation and metabolic reprogramming.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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, 1 synthesis or guideline pooled it.
- Pooled it
- EGFL9 regulates the growth and metastasis of hepatocellular carcinoma through EGFR/PI3K/AKT signaling pathway and amino acid modulation.Discover oncology · 2025Article
- TIM3Cancer cell · 2025Article
- Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation.Lipids in health and disease · 2024Article
- LncRNA mediated metabolic reprogramming: the chief culprits of solid tumor malignant progression: an update review.Nutrition & metabolism · 2024Review
- DLK1 and DLK2, two non-canonical ligands of NOTCH receptors, differentially modulate the osteogenic differentiation of mesenchymal C3H10T1/2 cells.Biological research · 2024Article
- Mitochondria: a new intervention target for tumor invasion and metastasis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Therapeutic protein PAK restrains the progression of triple negative breast cancer through degrading SREBP-1 mRNA.Breast cancer research : BCR · 2023Article
- Melatonin suppresses Akt/mTOR/S6K activity, induces cell apoptosis, and synergistically inhibits cell growth with sunitinib in renal carcinoma cells via reversing Warburg effect.Redox report : communications in free radical research · 2023Article
- The knockdown of lncRNA DLGAP1-AS2 suppresses osteosarcoma progression by inhibiting aerobic glycolysis via the miR-451a/HK2 axis.Cancer science · 2023Article
- Dlk2 interacts with Syap1 to activate Akt signaling pathway during osteoclast formation.Cell death & disease · 2023Article
- Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis.International journal of molecular sciences · 2023Review
- Glycolysis-related lncRNA TMEM105 upregulates LDHA to facilitate breast cancer liver metastasis via sponging miR-1208.Cell death & disease · 2023Article
- Alcohol dehydrogenase 4 is a TP53-associated gene signature for the prediction of prognosis in hepatocellular carcinoma.Oncology letters · 2023Article
- DDR2 coordinates EMT and metabolic reprogramming as a shared effector of FOXQ1 and SNAI1.Cancer research communications · 2022Article
- Haptoglobin Induces a Specific Proteomic Profile and a Mature-Associated Phenotype on Primary Human Monocyte-Derived Dendritic Cells.International journal of molecular sciences · 2022Article
- TGF-β induced reprogramming and drug resistance in triple-negative breast cells.BMC pharmacology & toxicology · 2022Article
- Different Expression Levels of DLK2 Inhibit NOTCH Signaling and Inversely Modulate MDA-MB-231 Breast Cancer Tumor Growth In Vivo.International journal of molecular sciences · 2022Article
- COA3 overexpression promotes non-small cell lung cancer metastasis by reprogramming glucose metabolism.American journal of cancer research · 2022Article
- RNA binding protein RBMS3 is a common EMT effector that modulates triple-negative breast cancer progression via stabilizing PRRX1 mRNA.Oncogene · 2021Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
The molecular mechanisms driving metastatic progression in triple-negative breast cancer (TNBC) patients are poorly understood. In this study, we demonstrate that epidermal growth factor-like 9 (EGFL9) is significantly upregulated in basal-like breast cancer cells and associated with metastatic progression in breast tumor samples. Functionally, EGFL9 is both necessary and sufficient to enhance cancer cell migration and invasion, as well as distant metastasis. Mechanistically, we demonstrate that EGFL9 binds cMET, activating cMET-mediated downstream signaling. EGFL9 and cMET co-localize at both the cell membrane and within the mitochondria. We further identify an interaction between EGFL9 and the cytochrome c oxidase (COX) assembly factor COA3. Consequently, EGFL9 regulates COX activity and modulates cell metabolism, promoting a Warburg-like metabolic phenotype. Finally, we show that combined pharmacological inhibition of cMET and glycolysis reverses EGFL9-driven stemness. Our results identify EGFL9 as a therapeutic target for combating metastatic progression in TNBC.
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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.