Evidence map›Paper›PMID 32072404›Full record

ArticleMolecular biology reports2020

Targeting signaling pathways of VEGFR1 and VEGFR2 as a potential target in the treatment of breast cancer.

Maryam Farzaneh Behelgardi, Saber Zahri, Zahra Gholami Shahvir, Farhad Mashayekhi, Laleh Mirzanejad, S Mohsen Asghari

Abstract read
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In one paragraph

Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 45 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Maryam Farzaneh BehelgardiDepartment of Biology, Faculty of Science, University of Mohaghegh Ardabili, Ardabil, Iran.
Saber ZahriDepartment of Biology, Faculty of Science, University of Mohaghegh Ardabili, Ardabil, Iran.
Zahra Gholami ShahvirDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran.
Farhad MashayekhiDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran.
Laleh MirzanejadDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran.
S Mohsen AsghariDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran. sm_asghari@guilan.ac.ir.ORCID http://orcid.org/0000-0002-0782-6687
University of Guilan · IRUniversity of Mohaghegh Ardabili · IRUniversity of Tehran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor angiogenesis allows tumor cells to grow and migrate toward the bloodstream and initiate metastasis. The interactions of vascular endothelial growth factors (VEGF) A and B, as the important regulating factors for blood vessel growth, with VEGFR1 and VEGFR2 trigger angiogenesis process. Thus, preventing these interactions led to the effective blockade of VEGF/VEGFRs signaling pathways. In this study, the inhibitory effect of a 23-mer linear peptide (VGB4), which binds to both VEGFR1 and VEGFR2, on VEGF-stimulated Human Umbilical Vein Endothelial Cells (HUVECs) and highly metastatic human breast cancer cell MDA-MB-231 proliferation was examined using MTT assay. To assess the anti-migratory potential of VGB4, HUVECs and also MDA-MB-231 cells wound healing assay was carried out at 48 and 72 h. In addition, downstream signaling pathways of VEGF associated with cell migration and invasion were investigated by quantification of mRNA and protein expression using real-time quantitative PCR and western blot in 4T1 tumor tissues and MDA-MB-231 cells. The results revealed that VGB4 significantly impeded proliferation of HUVECs and MDA-MB-231 cells, in a dose- and time-dependent manner, and migration of HUVECs and MDA-MB-231 cells for a prolonged time. We also observed statistically significant reduction of the transcripts and protein levels of focal adhesion kinase (FAK), Paxillin, matrix metalloproteinase-2 (MMP-2), RAS-related C3 botulinum substrate 1 (Rac1), P21-activated kinase-2 (PAK-2) and Cofilin-1 in VGB4-treated 4T1 tumor tissues compared to controls. The protein levels of phospho-VEGFR1, phospho-VEGFR2, Vimentin, β-catenin and Snail were markedly decreased in both VGB4-treated MDA-MB-231 cells and VGB4-treated 4T1 tumor tissues compared to controls as evidenced by western blotting. These results, in addition to our previous studies, confirm that dual blockage of VEGFR1 and VEGFR2, due to the inactivation of diverse signaling mediators, effectively suppresses tumor growth and metastasis.

Indexed as

Signal TransductionAnimalsBiomarkers, TumorBreast NeoplasmsCell Line, TumorChromatography, High Pressure LiquidDisease Models, AnimalFemaleGene ExpressionHumansMiceMolecular Targeted TherapyPeptidesrac GTP-Binding ProteinsRNA, MessengerVascular Endothelial Growth Factor Receptor-1Biomarkers, TumorPeptidesrac GTP-Binding ProteinsRNA, MessengerVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2Antagonist peptideBreast cancerMigrationVEGFVEGFR1VEGFR2

Identifiers

PMID32072404
OpenAlexW3008680920

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.