VEGFR-1 Regulates EGF-R to Promote Proliferation in Colon Cancer Cells

Autor: Naoko Yamagishi, Hikaru Nagano, Shigetada Teshima-Kondo, Chisato Tomida
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Placental growth factor
proliferation
Cell
Article
Catalysis
Inorganic Chemistry
lcsh:Chemistry
chemistry.chemical_compound
Paracrine signalling
vascular endothelial growth factor receptor-1 (vegfr-1)
Epidermal growth factor
medicine
Humans
Physical and Theoretical Chemistry
Autocrine signalling
Receptor
Molecular Biology
lcsh:QH301-705.5
Spectroscopy
Cell Proliferation
Placenta Growth Factor
Vascular Endothelial Growth Factor Receptor-1
Organic Chemistry
General Medicine
HCT116 Cells
Computer Science Applications
ErbB Receptors
Vascular endothelial growth factor
medicine.anatomical_structure
chemistry
vascular endothelial growth factor (vegf)
lcsh:Biology (General)
lcsh:QD1-999
Colonic Neoplasms
Cancer cell
Cancer research
epidermal growth factor receptor (egf-r)
colon cancer cells
hormones
hormone substitutes
and hormone antagonists
Signal Transduction
Zdroj: International Journal of Molecular Sciences, Vol 20, Iss 22, p 5608 (2019)
International Journal of Molecular Sciences
Volume 20
Issue 22
ISSN: 1422-0067
Popis: 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.
Databáze: OpenAIRE
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