Evidence map›Paper›PMID 27462783›Full record

ArticleOncotarget2016

MIEN1 drives breast tumor cell migration by regulating cytoskeletal-focal adhesion dynamics.

Marilyne Kpetemey, Pankaj Chaudhary, Timothy Van Treuren, Jamboor K Vishwanatha

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Marilyne KpetemeyDepartment of Molecular and Medical Genetics, Institute for Cancer Research, and The Texas Center for Health Disparities, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Pankaj ChaudharyDepartment of Molecular and Medical Genetics, Institute for Cancer Research, and The Texas Center for Health Disparities, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Timothy Van TreurenDepartment of Molecular and Medical Genetics, Institute for Cancer Research, and The Texas Center for Health Disparities, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Jamboor K VishwanathaDepartment of Molecular and Medical Genetics, Institute for Cancer Research, and The Texas Center for Health Disparities, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
University of North Texas · USUniversity of North Texas Health Science Center · US

Funding

Texas Minority Health, Research and Outreach (MiHERO)S21MD012472 · NIMHD · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI JAMBOOR K. VISHWANATHA · 2017 to 2026
$18.0M
Triple Negative Breast Cancer: Novel Biomarkers and Therapeutic StrategiesP20MD006882 · NIMHD · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI GHORPADE, ANUJA · 2012 to 2016
$5.8M
NIMHD NIH HHS P20 MD006882NIMHD NIH HHS S21 MD012472
6 · The paper itself

Abstract

Migration and invasion enhancer 1 (MIEN1) is an important regulator of cell migration and invasion. MIEN1 overexpression represents an oncogenic event that promotes tumor cell dissemination and metastasis. The underlying mechanism by which MIEN1 regulates migration and invasion has yet to be deciphered. Here, we demonstrate that MIEN1 acts as a cytoskeletal-signaling adapter protein to drive breast cancer cell migration. MIEN1 localization is concentrated underneath the actin-enriched protrusive structures of the migrating breast cancer cells. Depletion of MIEN1 led to the loss of actin-protrusive structures whereas the over-expression of MIEN1 resulted in rich and thick membrane extensions. Knockdown of MIEN1 also decreased the cell-substratum adhesion, suggesting a role for MIEN1 in actin cytoskeletal dynamics. Our results show that MIEN1 supports the transition of G-actin to F-actin polymerization and stabilizes F-actin polymers. Additionally, MIEN1 promotes cellular adhesion and actin dynamics by inducing phosphorylation of FAK at Tyr-925 and reducing phosphorylation of cofilin at Ser-3, which results in breast cancer cell migration. Collectively, our data show that MIEN1 plays an essential role in maintaining the plasticity of the dynamic membrane-associated actin cytoskeleton, which leads to an increase in cell motility. Hence, targeting MIEN1 might represent a promising means to prevent breast tumor metastasis.

Indexed as

Cell MovementFocal AdhesionsActin CytoskeletonActin Depolymerizing FactorsActinsBreast NeoplasmsCell AdhesionCell LineCell Line, TumorFocal Adhesion Kinase 1HumansIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsPhosphorylationPolymerizationRNA InterferenceActin Depolymerizing FactorsActinsFocal Adhesion Kinase 1Intracellular Signaling Peptides and ProteinsMIEN1 protein, humanNeoplasm ProteinsPTK2 protein, humanactin polymerizationcofilinfocal adhesion kinaseMIEN1migration

Identifiers

PMID27462783
PMCPMC5342390
OpenAlexW2490556211

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.