ArticleProceedings of the National Academy of Sciences of the United States of America2019
The VEGF receptor neuropilin 2 promotes homologous recombination by stimulating YAP/TAZ-mediated Rad51 expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Neural-tumor interactions: bidirectional regulatory mechanisms and nervous system-targeted tumor therapeutic strategies.Biomarker research · 2026Review
- Cisplatin resistance in an ovarian cancer model is mediated by microtubule dynamics regulator TPPP3 in synergy with tubulin code rewiring.Cell reports · 2026Article
- Discovery and Cryo-EM-Guided Development of a Neuropilin-2-Binding Aptamer for Receptor Antagonism.Journal of the American Chemical Society · 2026Article
- Targeting the ANGPTL4/NRP1/ABL1/RAD51 axis reverses cisplatin resistance by impairing DNA damage repair in head and neck cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- NCAPH-YAP1 interaction promotes breast cancer stemness and tumor progression.Stem cell research & therapy · 2025Article
- SOX5 inhibition overcomes PARP inhibitor resistance in BRCA-mutated breast and ovarian cancer.Cell death & disease · 2025Article
- Neuropilin-1: A Multifaceted Target for Cancer Therapy.Current oncology (Toronto, Ont.) · 2025Review
- Review
- "Brake" and "accelerator": revisiting tumor cell direct responses and the paradox of aggression in anti-VEGF therapy.Frontiers in immunology · 2025Review
- Expected and unexpected effects after systemic inhibition of Hippo transcriptional output in cancer.Nature communications · 2024Review
- YAP1-CPNE3 positive feedback pathway promotes gastric cancer cell progression.Cellular and molecular life sciences : CMLS · 2024Article
- Targeting the YAP/TAZ Hippo signaling pathway for oral cancer treatment.EXCLI journal · 2024Article
- Review
- Inhibition of VEGF binding to neuropilin-2 enhances chemosensitivity and inhibits metastasis in triple-negative breast cancer.Science translational medicine · 2023Article
- The oncogenic roles and clinical implications of YAP/TAZ in breast cancer.British journal of cancer · 2023Review
- Conditional expression of endorepellin in the tumor vasculature attenuates breast cancer growth, angiogenesis and hyaluronan deposition.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- The Hippo signaling pathway: from multiple signals to the hallmarks of cancers.Acta biochimica et biophysica Sinica · 2023Review
- The Hippo signaling pathway in gastric cancer.Acta biochimica et biophysica Sinica · 2023Review
- Deciphering the immunological and prognostic features of bladder cancer through platinum-resistance-related genes analysis and identifying potential therapeutic target P4HB.Frontiers in immunology · 2023Article
- Role of Neuropilin-2-mediated signaling axis in cancer progression and therapy resistance.Cancer metastasis reviews · 2022Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Vascular endothelial growth factor (VEGF) signaling in tumor cells mediated by neuropilins (NRPs) contributes to the aggressive nature of several cancers, including triple-negative breast cancer (TNBC), independently of its role in angiogenesis. Understanding the mechanisms by which VEGF-NRP signaling contributes to the phenotype of such cancers is a significant and timely problem. We report that VEGF-NRP2 promote homologous recombination (HR) in BRCA1 wild-type TNBC cells by contributing to the expression and function of Rad51, an essential enzyme in the HR pathway that mediates efficient DNA double-strand break repair. Mechanistically, we provide evidence that VEGF-NRP2 stimulates YAP/TAZ-dependent Rad51 expression and that Rad51 is a direct YAP/TAZ-TEAD transcriptional target. We also discovered that VEGF-NRP2-YAP/TAZ signaling contributes to the resistance of TNBC cells to cisplatin and that Rad51 rescues the defects in DNA repair upon inhibition of either VEGF-NRP2 or YAP/TAZ. These findings reveal roles for VEGF-NRP2 and YAP/TAZ in DNA repair, and they indicate a unified mechanism involving VEGF-NRP2, YAP/TAZ, and Rad51 that contributes to resistance to platinum chemotherapy.
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