Evidence map›Paper›PMID 26130964›Full record

ArticleJournal of Korean medical science2015

Antiangiogenic Activity of Acer tegmentosum Maxim Water Extract in Vitro and in Vivo.

Eok-Cheon Kim, So Hun Kim, Shan-Ji Piao, Tack-Joong Kim, Kiho Bae, Han Sung Kim, Soon-Sun Hong, Byoung Ick Lee, Moonsuk Nam

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Korean medical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Frontiers in pharmacology · 2024
    Article
  2. Nutrients · 2020
    Article
  3. Natural products against cancer angiogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
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

9 authors.

Eok-Cheon KimDivision of Biological Science and Technology and Yonsei-Fraunhofer Medical Device Lab., College of Science and Technology, Yonsei University, Wonju, Korea.
So Hun KimDivision of Endocrinology and Metabolism, Department of Internal Medicine, Inha University School of Medicine, Incheon, Korea.
Shan-Ji PiaoQingdao Endocrine & Diabetes Hospital, Qingdao, China.
Tack-Joong KimDivision of Biological Science and Technology and Yonsei-Fraunhofer Medical Device Lab., College of Science and Technology, Yonsei University, Wonju, Korea.
Kiho BaeDivision of Biological Science and Technology and Yonsei-Fraunhofer Medical Device Lab., College of Science and Technology, Yonsei University, Wonju, Korea.
Han Sung KimDepartment of Biomedical Engineering, Institute of Medical Engineering and Yonsei-Fraunhofer Medical Device Laboratory, Yonsei University, Wonju, Korea.
Soon-Sun HongDepartment of Biomedical Sciences, College of Medicine, Inha University, Incheon, Korea.
Byoung Ick LeeDepartment of Obstetrics & Gynecology, Inha University College of Medicine, Incheon, Korea.
Moonsuk NamDivision of Endocrinology and Metabolism, Department of Internal Medicine, Inha University School of Medicine, Incheon, Korea. ; Department of Clinical Pharmacology, Inha University School of Medicine, Incheon, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis, the formation of new blood vessels, is critical for tumor growth and metastasis. Notably, tumors themselves can lead to angiogenesis by inducing vascular endothelial growth factor (VEGF), which is one of the most potent angiogenic factors. Inhibition of angiogenesis is currently perceived as one of the most promising strategies for the blockage of tumor growth. In this study, we investigated the effects of Acer tegmentosum maxim water extract (ATME) on angiogenesis and its underlying signal mechanism. We studied the antiangiogenic activity of ATME by using human umbilical vein endothelial cells (HUVECs). ATME strongly inhibited VEGF-induced endothelial cell proliferation, migration, invasion, and tube formation, as well as vessel sprouting in a rat aortic ring sprouting assay. Moreover, we found that the p44/42 mitogen activated protein (MAP) kinase signaling pathway is involved in the inhibition of angiogenesis by ATME. Moreover, when we performed the in vivo matrigel plug assay, VEGF-induced angiogenesis was potently reduced when compared to that for the control group. Taken together, these results suggest that ATME exhibits potent antiangiogenic activity in vivo and in vitro and that these effects are regulated by the extracellular regulated kinase (ERK) pathway.

Indexed as

AcerAngiogenesis InhibitorsAnimalsCell Line, TumorCell MovementCell ProliferationCell SurvivalExtracellular Signal-Regulated MAP KinasesHep G2 CellsHumansHuman Umbilical Vein Endothelial CellsMAP Kinase Signaling SystemMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 1Neoplasm InvasivenessAngiogenesis InhibitorsExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase 1Nitric Oxide Synthase Type IIINOS3 protein, humanPlant ExtractsTranscription FactorsVascular Endothelial Growth Factor AVEGFA protein, humanWDR77 protein, humanAcer tegmentosum MaximAngiogenesisp44/42 MAP KinaseVascular Endothelial Growth Factor A

Identifiers

PMID26130964
PMCPMC4479955

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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.