Evidence map›Paper›PMID 28431393›Full record

ArticleOncotarget2017

Loss of Tpm4.1 leads to disruption of cell-cell adhesions and invasive behavior in breast epithelial cells via increased Rac1 signaling.

SukYeong Jeong, SunYoung Lim, Galina Schevzov, Peter W Gunning, David M Helfman

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. 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
0.4field-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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  6. Research Advances in the Role of the Tropomyosin Family in Cancer.International journal of molecular sciences · 2023
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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 2 countries.

SukYeong JeongDepartment of Biological Sciences, Korean Advanced Institute of Science and Technology, Daejeon, Republic of Korea.
SunYoung LimDepartment of Biological Sciences, Korean Advanced Institute of Science and Technology, Daejeon, Republic of Korea.
Galina SchevzovOncology Research Unit, School of Medical Sciences, UNSW, Sydney, NSW, Australia.
Peter W GunningOncology Research Unit, School of Medical Sciences, UNSW, Sydney, NSW, Australia.
David M HelfmanDepartment of Biological Sciences, Korean Advanced Institute of Science and Technology, Daejeon, Republic of Korea.
Korea Advanced Institute of Science and Technology · KRUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here we report the identification and characterization of a novel high molecular weight isoform of tropomyosin, Tpm4.1, expressed from the human TPM4 gene. Tpm4.1 expression is down-regulated in a subset of breast cancer cells compared with untransformed MCF10A breast epithelial cells and in highly metastatic breast cancer cell lines derived from poorly metastatic MDA-MD-231 cells. In addition, patients with invasive ductal breast carcinoma show decreased TPM4 expression compared with patients with ductal breast carcinoma in situ, and low TPM4 expression is associated with poor prognosis. Loss of Tpm4.1 using siRNA in MCF10A cells increases cell migration in wound-healing and Boyden chamber assays and invasion out of spheroids as well as disruption of cell-cell adhesions. Down-regulation of Tpm4.1 in MDA-MB-231 cells leads to disruption of actin organization and increased cell invasion and dissemination from spheroids into collagen gels. The down-regulation of Tpm4.1 induces Rac1-mediated alteration of myosin IIB localization, and pharmacologic inhibition of Rac1 or down-regulation of myosin IIB using siRNA inhibits the invasive phenotypes in MCF10A cells. Thus Tpm4.1 plays an important role in blocking invasive behaviors through Rac1-myosin IIB signaling and our findings suggest that decreased expression of Tpm4.1 might play a crucial role during tumor progression.

Indexed as

Signal TransductionActinsBreast NeoplasmsCell AdhesionCell Line, TumorCell MovementEpithelial CellsFemaleGene Expression Regulation, NeoplasticGene SilencingHumansIntercellular JunctionsNeoplasm InvasivenessNonmuscle Myosin Type IIBProtein IsoformsProtein TransportActinsNonmuscle Myosin Type IIBProtein Isoformsrac1 GTP-Binding ProteinTPM4 protein, humanTropomyosincell adhesionsinvasionmigrationTPM4tropomyosin

Identifiers

PMID28431393
PMCPMC5464889
OpenAlexW2604773248

What OpenQuestion holds

Textmetadata
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.