Evidence map›Paper›PMID 36499211›Full record

ArticleInternational journal of molecular sciences2022

Blockade of c-Met-Mediated Signaling Pathways by E7050 Suppresses Growth and Promotes Apoptosis in Multidrug-Resistant Human Uterine Sarcoma Cells.

Tsung-Teng Huang, Chuan-Mu Chen, Ying-Wei Lan, Song-Shu Lin, Kong-Bung Choo, Kowit-Yu Chong

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. 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 44% 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. 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

6 authors at 5 institutions in 3 countries.

Tsung-Teng HuangDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Chuan-Mu ChenDepartment of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 402, Taiwan.ORCID 0000-0003-2461-9150
Ying-Wei LanDivision of Pulmonary Biology, The Perinatal Institute of Cincinnati Children's Research Foundation, Cincinnati, OH 45229, USA.
Song-Shu LinDepartment of Nursing, Chang Gung University of Science and Technology, Taoyuan 33302, Taiwan.ORCID 0000-0003-3628-6875
Kong-Bung ChooCentre for Stem Cell Research, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Kajang 43000, Selangor, Malaysia.
Kowit-Yu ChongDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.ORCID 0000-0003-0974-0673
Chang Gung University · TWChang Gung University of Science and Technology · TWCincinnati Children's Hospital Medical Center · USNational Chung Hsing University · TWUniversiti Tunku Abdul Rahman · MY

Funding

Linkou Chang Gung Memorial Hospital CORPD-1K-0021Ministry of Science and Technology MOST-108-2314-B-182-052-MY3
6 · The paper itself

Abstract

E7050 is a potent inhibitor of c-Met receptor tyrosine kinase and has potential for cancer therapy. However, the underlying molecular mechanism involved in the anti-cancer property of E7050 has not been fully elucidated. The main objective of this study was to investigate the anti-tumor activity of E7050 in multidrug-resistant human uterine sarcoma MES-SA/Dx5 cells in vitro and in vivo, and to define its mechanisms. Our results revealed that E7050 reduced cell viability of MES-SA/Dx5 cells, which was associated with the induction of apoptosis and S phase cell cycle arrest. Additionally, E7050 treatment significantly upregulated the expression of Bax, cleaved PARP, cleaved caspase-3, p21, p53 and cyclin D1, while it downregulated the expression of survivin and cyclin A. On the other hand, the mechanistic study demonstrated that E7050 inhibited the phosphorylation of c-Met, Src, Akt and p38 in HGF-stimulated MES-SA/Dx5 cells. Further in vivo experiments showed that treatment of athymic nude mice carrying MES-SA/Dx5 xenograft tumors with E7050 remarkably suppressed tumor growth. E7050 treatment also decreased the expression of Ki-67 and p-Met, and increased the expression of cleaved caspase-3 in MES-SA/Dx5 tumor sections. Therefore, E7050 is a promising drug that can be developed for the treatment of multidrug-resistant uterine sarcoma.

Indexed as

SarcomaSoft Tissue NeoplasmsUterine NeoplasmsAminopyridinesAnimalsApoptosisCaspase 3Cell Line, TumorDrug Resistance, NeoplasmFemaleHumansMiceMice, NudePiperazinesProto-Oncogene Proteins c-metSignal TransductionAminopyridinesCaspase 3N-(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-metapoptosiscell cycle arrestc-MetE7050multidrug-resistant uterine sarcoma

Identifiers

PMID36499211
PMCPMC9740914
OpenAlexW4310172307

What OpenQuestion holds

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LicenceCC BY
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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.