ArticleeLife2017
Ambra1 spatially regulates Src activity and Src/FAK-mediated cancer cell invasion via trafficking networks.
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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.
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Who cites it
31 citing papers in PubMed, 39 citations in OpenAlex.
- Serum levels of FAK and some of its effectors in adult AML: correlation with prognostic factors and survival.Molecular and cellular biochemistry · 2021Trial
- Rab40 GTPases regulate AMBRA1-mediated transcription and cell migration.Journal of cell science · 2025Article
- Redox-Induced Stabilization of AMBRA1 by USP7 Promotes Intestinal Oxidative Stress and Colitis Through Antagonizing DUB3-Mediated NRF2 Deubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Autophagy-based therapy for hepatocellular carcinoma: from standard treatments to combination therapy, oncolytic virotherapy, and targeted nanomedicines.Clinical and experimental medicine · 2024Review
- Role of AMBRA1 in mitophagy regulation: emerging evidence in aging-related diseases.Autophagy · 2024Review
- IFITM3-mediated activation of TRAF6/MAPK/AP-1 pathways induces acquired TKI resistance in clear cell renal cell carcinoma.Investigative and clinical urology · 2024Article
- Roles and inhibitors of FAK in cancer: current advances and future directions.Frontiers in pharmacology · 2024Review
- Autophagy, molecular chaperones, and unfolded protein response as promoters of tumor recurrence.Cancer metastasis reviews · 2023Review
- Ambra1 in cancer: implications for clinical oncology.Apoptosis : an international journal on programmed cell death · 2022Review
- The Current State of Treatment and Future Directions in Cutaneous Malignant Melanoma.Biomedicines · 2022Review
- AMBRA1 and its role as a target for anticancer therapy.Frontiers in oncology · 2022Review
- IFITM protein regulation and functions: Far beyond the fight against viruses.Frontiers in immunology · 2022Review
- Chemoprevention of 4NQO-Induced Mouse Tongue Carcinogenesis by AKT Inhibitor through the MMP-9/RhoC Signaling Pathway and Autophagy.Analytical cellular pathology (Amsterdam) · 2022Article
- Targeting cancer stem cells in medulloblastoma by inhibiting AMBRA1 dual function in autophagy and STAT3 signalling.Acta neuropathologica · 2021Article
- Loss of Ambra1 promotes melanoma growth and invasion.Nature communications · 2021Article
- Targeting FAK in anticancer combination therapies.Nature reviews. Cancer · 2021Review
- Mitophagy in tumorigenesis and metastasis.Cellular and molecular life sciences : CMLS · 2021Review
- ECT2 promotes lung adenocarcinoma progression through extracellular matrix dynamics and focal adhesion signaling.Cancer science · 2021Article
- AMBRA1 and FAK1: crosstalking for improved targeted therapy in melanoma.Molecular & cellular oncology · 2021Article
- The Dual Role of Autophagy in Cancer Development and a Therapeutic Strategy for Cancer by Targeting Autophagy.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
Abstract
Here, using mouse squamous cell carcinoma cells, we report a completely new function for the autophagy protein Ambra1 as the first described 'spatial rheostat' controlling the Src/FAK pathway. Ambra1 regulates the targeting of active phospho-Src away from focal adhesions into autophagic structures that cancer cells use to survive adhesion stress. Ambra1 binds to both FAK and Src in cancer cells. When FAK is present, Ambra1 is recruited to focal adhesions, promoting FAK-regulated cancer cell direction-sensing and invasion. However, when Ambra1 cannot bind to FAK, abnormally high levels of phospho-Src and phospho-FAK accumulate at focal adhesions, positively regulating adhesion and invasive migration. Spatial control of active Src requires the trafficking proteins Dynactin one and IFITM3, which we identified as Ambra1 binding partners by interaction proteomics. We conclude that Ambra1 is a core component of an intracellular trafficking network linked to tight spatial control of active Src and FAK levels, and so crucially regulates their cancer-associated biological outputs.
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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.