Evidence map›Paper›PMID 29743493›Full record

ArticleScientific reports2018

The Kindlin-2 regulation of epithelial-to-mesenchymal transition in breast cancer metastasis is mediated through miR-200b.

Khalid Sossey-Alaoui, Elzbieta Pluskota, Dorota Szpak, William P Schiemann, Edward F Plow

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. Role of Kindlin 2 in prostate cancer.Scientific reports · 2024
    Article
  8. Article
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  12. Article
  13. Review
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  16. Review
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  19. Article
  20. Kindlins as modulators of breast cancer progression.Journal of breast cancer research · 2021
    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

5 authors at 2 institutions in 1 country.

Khalid Sossey-AlaouiDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. sosseyk@ccf.org.
Elzbieta PluskotaDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Dorota SzpakDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0003-2761-5489
William P SchiemannCase Comprehensive Cancer Center, Cleveland, OH, USA.
Edward F PlowDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Cleveland Clinic Lerner College of Medicine · USCase Comprehensive Cancer Center

Funding

Structure Basis for Talin-mediated Integrin ActivationP01HL073311 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI BYZOVA, TATIANA V · 2004 to 2019
$27.4M
Activation of the beta-3 integrins: Role of the KindlinsR01HL096062 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI PLOW, EDWARD FRANKLIN · 2009 to 2022
$5.6M
NHLBI NIH HHS P01 HL073311NHLBI NIH HHS R01 HL096062
6 · The paper itself

Abstract

Metastasis is the main cause of death in cancer patients, including breast cancer (BC). Despite recent progress in understanding the biological and molecular determinants of BC metastasis, effective therapeutic treatments are yet to be developed. Among the multitude of molecular mechanisms that regulate cancer metastasis, the epithelial-to-mesenchymal transition (EMT) program plays a key role in the activation of the biological steps leading to the metastatic phenotype. Kindlin-2 has been associated with the pathogenesis of several types of cancers, including BC. The role of Kindlin-2 in the regulation of BC metastasis, and to a lesser extent in EMT is not well understood. In this study, we show that Kindlin-2 is closely associated with the development of the metastatic phenotype in BC. We report that knockout of Kindlin-2 in either human or mouse BC cells, significantly inhibits metastasis in both human and mouse models of BC metastasis. We also report that the Kindlin-2-mediated inhibition of metastasis is the result of inhibition of expression of key molecular markers of the EMT program. Mechanistically, we show that miR-200b, a master regulator of EMT, directly targets and inhibits the expression of Kindlin-2, leading to the subsequent inhibition of EMT and metastasis. Together, our data support the targeting of Kindlin-2 as a therapeutic strategy against BC metastasis.

Indexed as

AnimalsBreast NeoplasmsCell AdhesionCell Line, TumorCytoskeletal ProteinsDisease ProgressionDown-RegulationEpithelial-Mesenchymal TransitionExtracellular MatrixFemaleFocal AdhesionsMiceMicroRNAsMuscle ProteinsNeoplasm MetastasisPodosomesCytoskeletal Proteinskindlin-2 protein, mouseMicroRNAsMirn200 microRNA, mouseMuscle Proteins

Identifiers

PMID29743493
PMCPMC5943603
OpenAlexW2800430194

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.