Evidence map›Paper›PMID 34196902›Full record

ArticleBreast cancer research and treatment2021

NEK5 activity regulates the mesenchymal and migratory phenotype in breast cancer cells.

Margarite D Matossian, Steven Elliott, T Van Hoang, Hope E Burks, Maryl K Wright, Madlin S Alzoubi, Thomas Yan, Tiffany Chang, Henri Wathieu, Gabrielle O Windsor and 11 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Breast cancer research and treatment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The NIMA-related kinase family and cancer.Frontiers in oncology · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022
    Review
  12. 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

21 authors at 3 institutions in 1 country.

Margarite D MatossianDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Steven ElliottDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
T Van HoangDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Hope E BurksDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Maryl K WrightDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Madlin S AlzoubiDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Thomas YanDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Tiffany ChangDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Henri WathieuDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Gabrielle O WindsorDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Alifiani Bo HartonoDepartment of Pathology, Tulane University School of Medicine, New Orleans, LA, USA.
Sean LeeDepartment of Pathology, Tulane University School of Medicine, New Orleans, LA, USA.
William J ZuercherStructural Genomics Consortium, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
David H DrewryStructural Genomics Consortium, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Carrow WellsStructural Genomics Consortium, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Nirav KapadiaStructural Genomics Consortium, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Aaron BuechleinIndiana University Center for Genomics and Bioinformatics, Bloomington, IN, USA.
Fang FangIndiana University Center for Genomics and Bioinformatics, Bloomington, IN, USA.
Kenneth P NephewIndiana University Center for Genomics and Bioinformatics, Bloomington, IN, USA.
Bridgette M Collins-BurowDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Matthew E BurowDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA. mburow@tulane.edu.ORCID http://orcid.org/0000-0002-0642-6630
Tulane University · USUniversity of North Carolina at Chapel Hill · USIndiana University Bloomington · US

Funding

MEK5-Erk5 in breast cancer resistanceR01CA125806 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI BUROW, MATTHEW E. · 2010 to 2014
$1.5M
Characterization of an understudied kinase, NEK5, in acquisition of a mesenchymaland migratory cell phenotypeR03TR003386 · NCATS · TULANE UNIVERSITY OF LOUISIANA · PI BUROW, MATTHEW E., DREWRY, DAVID HAROLD · 2020 to 2020
$167k
NCATS NIH HHS 1R03TR003386-01NCATS NIH HHS R03 TR003386NCI NIH HHS R01CA125806NIH HHS R01-CA174785-01A1
6 · The paper itself

Abstract

purposeBreast cancer remains a prominent global disease affecting women worldwide despite the emergence of novel therapeutic regimens. Metastasis is responsible for most cancer-related deaths, and acquisition of a mesenchymal and migratory cancer cell phenotypes contributes to this devastating disease. The utilization of kinase targets in drug discovery have revolutionized the field of cancer research but despite impressive advancements in kinase-targeting drugs, a large portion of the human kinome remains understudied in cancer. NEK5, a member of the Never-in-mitosis kinase family, is an example of such an understudied kinase. Here, we characterized the function of NEK5 in breast cancer.

methodsStably overexpressing NEK5 cell lines (MCF7) and shRNA knockdown cell lines (MDA-MB-231, TU-BcX-4IC) were utilized. Cell morphology changes were evaluated using immunofluorescence and quantification of cytoskeletal components. Cell proliferation was assessed by Ki-67 staining and transwell migration assays tested cell migration capabilities. In vivo experiments with murine models were necessary to demonstrate NEK5 function in breast cancer tumor growth and metastasis.

resultsNEK5 activation altered breast cancer cell morphology and promoted cell migration independent of effects on cell proliferation. NEK5 overexpression or knockdown does not alter tumor growth kinetics but promotes or suppresses metastatic potential in a cell type-specific manner, respectively.

conclusionWhile NEK5 activity modulated cytoskeletal changes and cell motility, NEK5 activity affected cell seeding capabilities but not metastatic colonization or proliferation in vivo. Here we characterized NEK5 function in breast cancer systems and we implicate NEK5 in regulating specific steps of metastatic progression.

Indexed as

Breast NeoplasmsNIMA-Related KinasesAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleHumansMicePhenotypeRNA, Small InterferingNEK5 protein, humanNIMA-Related KinasesRNA, Small InterferingBreast cancerCell motilityKinase targetMesenchymal phenotypeMetastasisNever-in-mitosis A-related kinase

Identifiers

PMID34196902
OpenAlexW3163142692

What OpenQuestion holds

Textmetadata
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.