ArticleFEBS open bio2023
Reduced FRG1 expression promotes angiogenesis via activation of the FGF2-mediated ERK/AKT pathway.
Article in FEBS open bio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- FGFR2 is a Crucial Factor for Adipose-Derived Mesenchymal Stem Cells in Promoting Diabetic Foot Ulcer Healing Through Angiogenesis.Journal of cellular and molecular medicine · 2025Article
- Polystyrene microplastics impair the function of human retinal microvascular endothelial cells and pericytes and increase vascular permeabilityFrontiers in medicine · 2025Article
- Unveiling FRG1's DNA repair role in breast cancer.Scientific reports · 2024Article
- Molecular diagnostic yield of whole-exome sequencing in Saudi autistic children with epilepsy.International journal of health sciencesArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Identifying novel targets that control both tumorigenesis and angiogenesis can aid in developing a more potent anti-angiogenic therapeutic strategy. We previously reported that reduction of FRG1 is associated with increased p38-MAPK signaling in prostate cancer and with elevated MEK-ERK signaling in breast cancer. Here, we reveal the role of FRG1 in tumor angiogenesis. Our findings demonstrate that depleted FRG1 levels enhance the proliferation, migration, and tubule formation of HUVECs in a paracrine manner, and this was further substantiated in multiple animal models. Mechanistically, FRG1 depletion activated the expression of FGF2 in breast cancer cells, which triggered the ERK/AKT cascade in endothelial cells. As FRG1 affects multiple tumorigenic properties and it is upstream of FGF2, it can be explored as a therapeutic target that is less prone to resistance.
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Registered trials
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