Evidence map›Paper›PMID 37298555›Full record

ArticleInternational journal of molecular sciences2023

E7050 Suppresses the Growth of Multidrug-Resistant Human Uterine Sarcoma by Inhibiting Angiogenesis via Targeting of VEGFR2-Mediated Signaling Pathways.

Tsung-Teng Huang, Chuan-Mu Chen, Song-Shu Lin, Ying-Wei Lan, Hsu-Chen Cheng, Kong-Bung Choo, Ching-Chiung Wang, Tse-Hung Huang, Kowit-Yu Chong

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. 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 at 6 institutions in 3 countries.

Tsung-Teng HuangSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.
Chuan-Mu ChenDepartment of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.ORCID 0000-0003-2461-9150
Song-Shu LinDepartment of Nursing, Chang Gung University of Science and Technology, Taoyuan 33302, Taiwan.ORCID 0000-0003-3628-6875
Ying-Wei LanDivision of Pulmonary Biology, The Perinatal Institute of Cincinnati Children's Research Foundation, Cincinnati, OH 45229, USA.
Hsu-Chen ChengDepartment of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.
Kong-Bung ChooCentre for Stem Cell Research, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Kajang 43000, Selangor, Malaysia.
Ching-Chiung WangSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.
Tse-Hung HuangDepartment of Traditional Chinese Medicine, Linkou Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan.ORCID 0000-0002-5231-9932
Kowit-Yu ChongTraditional Herbal Medicine Research Center, Taipei Medical University Hospital, Taipei 11031, Taiwan.ORCID 0000-0003-0974-0673
Chang Gung University · TWNational Chung Hsing University · TWChang Gung University of Science and Technology · TWCincinnati Children's Hospital Medical Center · USTaipei Medical University Hospital · TWUniversiti Tunku Abdul Rahman · MY

Funding

Chang Gung Memorial Hospital CMRPD-1L-0132Ministry of Science and Technology of Taiwan MOST-111-2314-B-182-057
6 · The paper itself

Abstract

E7050 is an inhibitor of VEGFR2 with anti-tumor activity; however, its therapeutic mechanism remains incompletely understood. In the present study, we aim to evaluate the anti-angiogenic activity of E7050 in vitro and in vivo and define the underlying molecular mechanism. It was observed that treatment with E7050 markedly inhibited proliferation, migration, and capillary-like tube formation in cultured human umbilical vein endothelial cells (HUVECs). E7050 exposure in the chick embryo chorioallantoic membrane (CAM) also reduced the amount of neovessel formation in chick embryos. To understand the molecular basis, E7050 was found to suppress the phosphorylation of VEGFR2 and its downstream signaling pathway components, including PLCγ1, FAK, Src, Akt, JNK, and p38 MAPK in VEGF-stimulated HUVECs. Moreover, E7050 suppressed the phosphorylation of VEGFR2, FAK, Src, Akt, JNK, and p38 MAPK in HUVECs exposed to MES-SA/Dx5 cells-derived conditioned medium (CM). The multidrug-resistant human uterine sarcoma xenograft study revealed that E7050 significantly attenuated the growth of MES-SA/Dx5 tumor xenografts, which was associated with inhibition of tumor angiogenesis. E7050 treatment also decreased the expression of CD31 and p-VEGFR2 in MES-SA/Dx5 tumor tissue sections in comparison with the vehicle control. Collectively, E7050 may serve as a potential agent for the treatment of cancer and angiogenesis-related disorders.

Indexed as

SarcomaSignal TransductionVascular Endothelial Growth Factor Receptor-2AminopyridinesAngiogenesis InhibitorsAnimalsCell MovementCell ProliferationChick EmbryoHumansHuman Umbilical Vein Endothelial CellsNeovascularization, PathologicPiperazinesProto-Oncogene Proteins c-aktAminopyridinesAngiogenesis InhibitorsN-(2-fluoro-4-((2-(4-(4-methylpiperazin-1-yl)piperidin-1-yl)carbonylaminopyridin-4-yl)oxy)phenyl)-N'-(4-fluorophenyl)cyclopropane-1,1-dicarboxamidePiperazinesProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor Receptor-2angiogenesisE7050multidrug-resistant human uterine sarcomaVEGFVEGFR2

Identifiers

PMID37298555
PMCPMC10253979
OpenAlexW4379052123

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.