Evidence map›Paper›PMID 26849234›Full record

ArticleOncotarget2016

NMU signaling promotes endometrial cancer cell progression by modulating adhesion signaling.

Ting-Yu Lin, Fang-Ju Wu, Chia-Lin Chang, Zhongyou Li, Ching-Wei Luo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  8. Neuromedin U induces an invasive phenotype in CRC cells expressing the NMUR2 receptor.Journal of experimental & clinical cancer research : CR · 2021
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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

5 authors at 2 institutions in 1 country.

Ting-Yu LinDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
Fang-Ju WuDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
Chia-Lin ChangDepartment of Obstetrics and Gynecology, Chang Gung Memorial Hospital Linkou Medical Center, Chang Gung University, Kweishan, Taoyuan 333, Taiwan.
Zhongyou LiDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
Ching-Wei LuoDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
National Yang Ming Chiao Tung University · TWChang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuromedin U (NMU) was originally named based on its strong uterine contractile activity, but little is known regarding its signaling/functions in utero. We identified that NMU and one of its receptors, NMUR2, are not only present in normal uterine endometrium but also co-expressed in endometrial cancer tissues, where the NMU level is correlated with the malignant grades and survival of patients. Cell-based assays further confirmed that NMU signaling can promote cell motility and proliferation of endometrial cancer cells derived from grade II tumors. Activation of NMU pathway in these endometrial cancer cells is required in order to sustain expression of various adhesion molecules, such as CD44 and integrin alpha1, as well as production of their corresponding extracellular matrix ligands, hyaluronan and collagen IV; it also increased the activity of SRC and its downstream proteins RHOA and RAC1. Thus, it is concluded that NMU pathway positively controls the adhesion signaling-SRC-Rho GTPase axis in the tested endometrial cancer cells and that changes in cell motility and proliferation can occur when there is manipulation of NMU signaling in these cells either in vitro or in vivo. Intriguingly, this novel mechanism also explains how NMU signaling promotes the EGFR-driven and TGFβ receptor-driven mesenchymal transitions. Through the above axis, NMU signaling not only can promote malignancy of the tested endometrial cancer cells directly, but also helps these cells to become more sensitive to niche growth factors in their microenvironment.

Indexed as

AnimalsCell AdhesionCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticCollagenDisease ProgressionEndometrial NeoplasmsEndometriumFemaleHumansHyaluronan ReceptorsHyaluronic AcidIntegrin alpha1MiceCD44 protein, humanCollagenHyaluronan ReceptorsHyaluronic AcidIntegrin alpha1neuromedin Uneuromedin U receptorNeuropeptidesrac1 GTP-Binding ProteinRAC1 protein, humanReceptors, NeurotransmitterrhoA GTP-Binding ProteinRHOA protein, humansrc-Family Kinasesadhesion signalingendometrial cancerG protein-coupled receptorneuromedin UNMUR2

Identifiers

PMID26849234
PMCPMC4891116
OpenAlexW2291973388

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Registered trials

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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.