ArticlePloS one2016
EGF-Induced VEGF Exerts a PI3K-Dependent Positive Feedback on ERK and AKT through VEGFR2 in Hematological In Vitro Models.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
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- Three-Dimensional Growth of Prostate Cancer Cells Exposed to Simulated Microgravity.Frontiers in cell and developmental biology · 2022Article
- B-cell clonogenic activity of HIV-1 p17 variants is driven by PAR1-mediated EGF transactivation.Cancer gene therapy · 2021Article
- Targeting K-Ras and apoptosis-driven cellular transformation in cancer.Cell death discovery · 2021Review
- KCNN4 promotes the progression of lung adenocarcinoma by activating the AKT and ERK signaling pathways.Cancer biomarkers : section A of Disease markers · 2021Article
- Transcriptional Activation of MYC-Induced Genes by GCN5 Promotes B-cell Lymphomagenesis.Cancer research · 2020Article
- VEGF-A in Cardiomyocytes and Heart Diseases.International journal of molecular sciences · 2020Review
- Osteoking improves OP rat by enhancing HSP90‑β expression.International journal of molecular medicine · 2020Article
- Autocrine VEGF signalling on M2 macrophages regulates PD-L1 expression for immunomodulation of T cells.Journal of cellular and molecular medicine · 2019Article
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- Hsp90β promoted endothelial cell-dependent tumor angiogenesis in hepatocellular carcinoma.Molecular cancer · 2017Article
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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
EGFR and VEGFR pathways play major roles in solid tumor growth and progression, however, little is known about these pathways in haematological tumors. This study investigated the crosstalk between EGFR and VEGFR2 signaling in two hematological in vitro models: THP1, a human monocytic leukemia, and Raji, a Burkitt's lymphoma, cell lines. Results showed that both cell lines express EGFR and VEGFR2 and responded to EGF stimulation by activating EGFR, triggering VEGF production and phosphorylating ERK, AKT, and p38 very early, with a peak of expression at 10-20min. Blocking EGFR using Tyrphostin resulted in inhibiting EGFR induced activation of ERK, AKT, and p38. In addition, EGF stimulation caused a significant and immediate increase, within 1min, in pVEGFR2 in both cell lines, which peaked at ~5-10 min after treatment. Selective inhibition of VEGFR2 by DMH4, anti-VEGFR2 antibody or siRNA diminished EGF-induced pAKT and pERK, indicating a positive feedback exerted by EGFR-induced VEGF. Similarly, the specific PI3K inhibitor LY294002, suppressed AKT and ERK phosphorylation showing that VEGF feedback is PI3K-dependent. On the other hand, phosphorylation of p38, initiated by EGFR and independent of VEGF feedback, was diminished using PLC inhibitor U73122. Moreover, measurement of intracellular [Ca2+] and ROS following VEGFR2 inhibition and EGF treatment proved that VEGFR2 is not implicated in EGF-induced Ca2+ release whereas it boosts EGF-induced ROS production. Furthermore, a significant decrease in pAKT, pERK and p-p38 was shown following the addition of the ROS inhibitor NAC. These results contribute to the understanding of the crosstalk between EGFR and VEGFR in haematological malignancies and their possible combined blockade in therapy.
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