ArticleOncogene2017
Elevation of adenylate energy charge by angiopoietin-like 4 enhances epithelial-mesenchymal transition by inducing 14-3-3γ expression.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 68 citations in OpenAlex.
- Angiopoietin-like protein 4 deficiency promotes tumor immune infiltration and CD8Molecular therapy. Oncology · 2026Article
- Patient-derived orthotopic xenograft models recapitulate the peritoneal dissemination of pancreatic cancer and delineate its transcriptional and regulatory programs.Journal of experimental & clinical cancer research : CR · 2026Article
- YWHAG overexpression correlates with an immune-desert microenvironment and poor prognosis in laryngeal squamous cell carcinoma.Frontiers in immunology · 2026Article
- Energy Metabolism Profiling of Human Colorectal Tumours.Journal of cellular and molecular medicine · 2025Article
- Adipose Factor ANGPTL4: Its Role in Aging Mechanisms and Associated Diseases.Clinical interventions in aging · 2025Review
- ANGPTL4 promotes choroidal neovascularization and subretinal fibrosis through the endothelial‒mesenchymal transition.International ophthalmology · 2024Article
- Age-related epithelial defects limit thymic function and regeneration.Nature immunology · 2024Article
- YWHAG promotes colorectal cancer progression by regulating the CTTN-Wnt/β-catenin signaling axis.Medical oncology (Northwood, London, England) · 2024Article
- Optimizing Phosphopeptide Structures That Target 14-3-3ε in Cutaneous Squamous Cell Carcinoma.ACS omega · 2024Article
- Establishment of a prognostic model for hypoxia-associated genes in OPSCC and revelation of intercellular crosstalk.Frontiers in immunology · 2024Article
- YWHAG Deficiency Disrupts the EMT-Associated Network to Induce Oxidative Cell Death and Prevent Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Optimizing Phosphopeptide Structures That Target 14-3-3ε in Cutaneous Squamous Cell Carcinoma.bioRxiv : the preprint server for biology · 2023Article
- Transcriptomic and functional analysis of ANGPTL4 overexpression in pancreatic cancer nominates targets that reverse chemoresistance.BMC cancer · 2023Article
- Spatial probabilistic mapping of metabolite ensembles in mass spectrometry imaging.Nature communications · 2023Article
- Transcriptomic and functional analysis of ANGPTL4 overexpression in pancreatic cancer nominates targets that reverse chemoresistance.Research square · 2023Article
- Angiopoietin-like 4 promotes glucose metabolism by regulating glucose transporter expression in colorectal cancer.Journal of cancer research and clinical oncology · 2022Article
- Fusobacterium nucleatum promotes colon cancer progression by changing the mucosal microbiota and colon transcriptome in a mouse model.World journal of gastroenterology · 2022Article
- STAT3 induces breast cancer growth via ANGPTL4, MMP13 and STC1 secretion by cancer associated fibroblasts.Oncogene · 2022Article
- Article
- ANGPTL4-Mediated Promotion of Glycolysis Facilitates the Colonization ofCancer research · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastatic cancer cells acquire energy-intensive processes including increased invasiveness and chemoresistance. However, how the energy demand is met and the molecular drivers that coordinate an increase in cellular metabolic activity to drive epithelial-mesenchymal transition (EMT), the first step of metastasis, remain unclear. Using different in vitro and in vivo EMT models with clinical patient's samples, we showed that EMT is an energy-demanding process fueled by glucose metabolism-derived adenosine triphosphate (ATP). We identified angiopoietin-like 4 (ANGPTL4) as a key player that coordinates an increase in cellular energy flux crucial for EMT via an ANGPTL4/14-3-3γ signaling axis. This augmented cellular metabolic activity enhanced metastasis. ANGPTL4 knockdown suppresses an adenylate energy charge elevation, delaying EMT. Using an in vivo dual-inducible EMT model, we found that ANGPTL4 deficiency reduces cancer metastasis to the lung and liver. Unbiased kinase inhibitor screens and Ingenuity Pathway Analysis revealed that ANGPTL4 regulates the expression of 14-3-3γ adaptor protein via the phosphatidylinositol-3-kinase/AKT and mitogen-activated protein kinase signaling pathways that culminate to activation of transcription factors, CREB, cFOS and STAT3. Using a different mode of action, as compared with protein kinases, the ANGPTL4/14-3-3γ signaling axis consolidated cellular bioenergetics and stabilized critical EMT proteins to coordinate energy demand and enhanced EMT competency and metastasis, through interaction with specific phosphorylation signals on target proteins.
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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.