ArticleInternational journal of molecular sciences2019
VEGFR-1 Regulates EGF-R to Promote Proliferation in Colon Cancer Cells.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
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- Ileal perforation at the site of peritoneal metastasis with intestinal infiltration by dual EGFR-VEGF pathway inhibition in an EGFR-mutant non-small cell lung cancer patient.International cancer conference journal · 2024Article
- Construction and Validation of a Protein-associated Prognostic Model for Gastrointestinal Cancer.Combinatorial chemistry & high throughput screening · 2023Article
- Cancer-Associated Membrane Protein as Targeted Therapy for Bladder Cancer.Pharmaceutics · 2022Review
- Exploring the Mechanism and Suggesting Combination Therapies for HDAC Inhibitors in Androgen Receptor-Null Prostate Cancer Using Multivariate Statistical Analysis and Data Mining Techniques.Bioinformatics and biology insights · 2022Article
- Novel Xanthone Derivatives Impair Growth and Invasiveness of Colon Cancer Cells In Vitro.Biomolecules · 2021Article
- HOTAIR regulates colorectal cancer stem cell properties and promotes tumorigenicity by sponging miR-211-5p and modulating FLT-1.Cell cycle (Georgetown, Tex.) · 2021Article
- Identifying Novel Actionable Targets in Colon Cancer.Biomedicines · 2021Review
- Molecular and Translational Research on Colorectal Cancer.International journal of molecular sciences · 2020Article
- Inhibition ofBioMed research international · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relationship between epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) pathways in tumor growth is well established. EGF induces VEGF production in cancer cells, and the paracrine VEGF activates vascular endothelial cells to promote tumor angiogenesis and thus supports tumor cell growth in an angiogenesis-dependent manner. In this study, we found angiogenesis-independent novel crosstalk between the VEGF and the EGF pathways in the regulation of colon cancer cell proliferation. Stimulation of colon cancer cells with VEGF-A and placental growth factor (PlGF) activated VEGF receptor-1 (VEGFR-1) and increased proliferation activity in an autocrine EGF/EGF receptor (EGF-R)-dependent manner. Mechanistically, VEGFR-1 interacted with and stabilized EGF-R, leading to increased EGF-R protein levels and prolonged its expression on cell surface plasma membrane. In contrast, VEGFR-1 blockade by a neutralizing antibody and an antagonistic peptide of VEGFR-1 suppressed the complex formation of VEGFR-1 and EGF-R and decreased EGF-R expression via a lysosome-dependent pathway, resulting in the suppression of proliferation activity. Our results indicated that VEGFR-1 regulated EGF-R expression to promote proliferation activity in a cell-autonomous-dependent manner.
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Registered trials
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