Evidence map›Paper›PMID 29316206›Full record

ArticleMolecular oncology2018

Inhibition of VEGF-dependent angiogenesis and tumor angiogenesis by an optimized antibody targeting CLEC14a.

Taek-Keun Kim, Chang Sik Park, Jihye Jang, Mi Ra Kim, Hee-Jun Na, Kangseung Lee, Hyun Jung Kim, Kyun Heo, Byong Chul Yoo, Young-Myeong Kim and 7 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-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

24 citing papers in PubMed, 44 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

17 authors at 4 institutions in 1 country.

Taek-Keun KimScripps Korea Antibody Institute, Chuncheon, South Korea.
Chang Sik ParkScripps Korea Antibody Institute, Chuncheon, South Korea.
Jihye JangScripps Korea Antibody Institute, Chuncheon, South Korea.
Mi Ra KimScripps Korea Antibody Institute, Chuncheon, South Korea.
Hee-Jun NaScripps Korea Antibody Institute, Chuncheon, South Korea.
Kangseung LeeScripps Korea Antibody Institute, Chuncheon, South Korea.
Hyun Jung KimResearch Institute, National Cancer Center, Goyang, South Korea.
Kyun HeoResearch Institute, National Cancer Center, Goyang, South Korea.
Byong Chul YooResearch Institute, National Cancer Center, Goyang, South Korea.
Young-Myeong KimDepartment of Molecular and Cellular Biochemistry, Kangwon National University, Chuncheon, South Korea.
Je-Wook LeeNew Drug Development Center, Osong Medical Innovation Foundation, South Korea.
Su Jin KimNew Drug Development Center, Osong Medical Innovation Foundation, South Korea.
Eun Sung KimNew Drug Development Center, Osong Medical Innovation Foundation, South Korea.
Dae Young KimNew Drug Development Center, Osong Medical Innovation Foundation, South Korea.
Kiweon ChaNew Drug Development Center, Osong Medical Innovation Foundation, South Korea.
Tae Gyu LeeNew Drug Development Center, Osong Medical Innovation Foundation, South Korea.
Sukmook LeeScripps Korea Antibody Institute, Chuncheon, South Korea.
Scripps Korea Antibody Institute · KROsong Medical Innovation Foundation · KRNational Cancer Center · KRKangwon National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The C-type lectin-like domain of CLEC14a (CLEC14a-C-type lectin-like domain [CTLD]) is a key domain that mediates endothelial cell-cell contacts in angiogenesis. However, the role of CLEC14a-CTLD in pathological angiogenesis has not yet been clearly elucidated. In this study, through complementarity-determining region grafting, consecutive deglycosylation, and functional isolation, we generated a novel anti-angiogenic human monoclonal antibody that specifically targets CLEC14a-CTLD and that shows improved stability and homogeneity relative to the parental antibody. We found that this antibody directly inhibits CLEC14a-CTLD-mediated endothelial cell-cell contact and simultaneously downregulates expression of CLEC14a on the surface of endothelial cells. Using various in vitro and in vivo functional assays, we demonstrated that this antibody effectively suppresses vascular endothelial growth factor (VEGF)-dependent angiogenesis and tumor angiogenesis of SNU182 human hepatocellular carcinoma, CFPAC-1 human pancreatic cancer, and U87 human glioma cells. Furthermore, we also found that this antibody significantly inhibits tumor angiogenesis of HCT116 and bevacizumab-adapted HCT116 human colorectal cancer cells. These findings suggest that antibody targeting of CLEC14a-CTLD has the potential to suppress VEGF-dependent angiogenesis and tumor angiogenesis and that CLEC14a-CTLD may be a novel anti-angiogenic target for VEGF-dependent angiogenesis and tumor angiogenesis.

Indexed as

AnimalsAntibodies, MonoclonalCell Adhesion MoleculesCell CommunicationCell Line, TumorFemaleHCT116 CellsHumansHuman Umbilical Vein Endothelial CellsImmunoglobulin GLectins, C-TypeMiceMice, Inbred BALB CMice, NudeNeovascularization, PathologicNeovascularization, PhysiologicAntibodies, MonoclonalCell Adhesion MoleculesCLEC14A protein, humanImmunoglobulin GLectins, C-TypeVascular Endothelial Growth Factor AVEGFA protein, humanangiogenesisCLEC14aCTLDtumor angiogenesisVEGF

Identifiers

PMID29316206
PMCPMC5830631
OpenAlexW2784044597

What OpenQuestion holds

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LicenceCC BY
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.