Evidence map›Paper›PMID 26693066›Full record

ArticleAmerican journal of cancer research2015

A VEGFR1 antagonistic peptide inhibits tumor growth and metastasis through VEGFR1-PI3K-AKT signaling pathway inhibition.

Zheng Zhou, Chuanke Zhao, Lixin Wang, Xiaodan Cao, Jian Li, Ruijing Huang, Qiaocong Lao, Hangping Yu, Yanna Li, Haiyan Du and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  6. Inhibitory Effects ofEvidence-based complementary and alternative medicine : eCAM · 2021
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  12. Correlation amongTranslational cancer research · 2020
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. ACS medicinal chemistry letters · 2017
    Article
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

12 authors at 4 institutions in 3 countries.

Zheng ZhouDepartment of Biochemistry and Molecular Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute Beijing, China.
Chuanke ZhaoDepartment of Biochemistry and Molecular Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute Beijing, China.
Lixin WangDepartment of Biochemistry and Molecular Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute Beijing, China.
Xiaodan CaoTasly Holding Group Tianjin, China.
Jian LiTasly Holding Group Tianjin, China.
Ruijing HuangTasly Holding Group Tianjin, China.
Qiaocong LaoHunter Biotechnology Corporation Hangzhou, China.
Hangping YuHunter Biotechnology Corporation Hangzhou, China.
Yanna LiDepartment of Obstetrics & Gynecology, Beijing Anzhen Hospital, Capital Medical University; Beijing Institute of Heart, Lung and Blood Vessel Diseases Beijing, China.
Haiyan DuDrug Clinical Trail Institution, Beijing Anzhen Hospital, Capital Medical University Beijing, China.
Like QuDepartment of Biochemistry and Molecular Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute Beijing, China.
Chengchao ShouDepartment of Biochemistry and Molecular Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute Beijing, China.
Ministry of Education · ETTasly Holding Group (China) · CNBeijing Anzhen Hospital · CNThe Hunterian · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is central to the growth of cancers and VEGFR-1/Flt-1 plays an important role during the neovascularization under pathological conditions. We previously founded a VEGFR1 antagonistic peptide, F56, by screening the phage peptide library. We showed that DHFR-F56 chimeric protein displayed anti-tumor activity and inhibited angiogenesis, however the anti-tumor activity of monomeric F56 and the mechanism remain unclear. In this study, we found that the F56 didn't affect VEGF-A induced endothelial cell proliferation, but reduced migration and tube formation of endothelial cells. F56 also inhibited the sprout of rat aortic endothelial cells, the angiogenesis of chicken embryo chorioallantoic membrane as well as the generation of subintestinal vein vessels (SIV) in zebrafish embryos. We found that F56 inhibited VEGF-induced phosphorylation of VEGFR1, as well as the phosphorylation of the downstream of PI3K-AKT axis. However, F56 had no effect on the phosphorylation of VEGFR2. Correlating with these effects, F56 inhibited xenograft growth of HT-29 and MGC-823 cells in BALB/c nude mice, and significantly suppressed the lung metastasis of B16 cells in C57BL/6 mice. Our study demonstrated that monomeric peptide F56 had a significant anti-tumor activity by inhibiting angiogenesis, and laid the foundation for its clinical application.

Indexed as

angiogenesisendothelial cellsmetastasisPeptidePI3K/AktVEGFR1

Identifiers

PMID26693066
PMCPMC4656737
OpenAlexW2303764417

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.