Evidence map›Paper›PMID 36550548›Full record

ArticleCell communication and signaling : CCS2022

Identification of biological pathways and processes regulated by NEK5 in breast epithelial cells via an integrated proteomic approach.

Camila de Castro Ferezin, Terry C C Lim Kam Sian, Yunjian Wu, Xiuquan Ma, Anderly C Chüeh, Cheng Huang, Ralf B Schittenhelm, Jörg Kobarg, Roger J Daly

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Mitochondria transcription and cancer.Cell death discovery · 2024
    Review
  6. Review
  7. 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

9 authors at 3 institutions in 2 countries.

Camila de Castro FerezinCancer Program, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, 3800, Australia.
Terry C C Lim Kam SianCancer Program, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, 3800, Australia.
Yunjian WuCancer Program, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, 3800, Australia.
Xiuquan MaCancer Program, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, 3800, Australia.
Anderly C ChüehCancer Program, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, 3800, Australia.
Cheng HuangDepartment of Biochemistry and Molecular Biology, Monash University, Melbourne, VIC, 3800, Australia.
Ralf B SchittenhelmDepartment of Biochemistry and Molecular Biology, Monash University, Melbourne, VIC, 3800, Australia.
Jörg KobargFaculty of Pharmaceutical Sciences, State University of Campinas, São Paulo, Brazil.
Roger J DalyCancer Program, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, 3800, Australia. roger.daly@monash.edu.
Monash University · AUAustralian Regenerative Medicine Institute · AUUniversidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Specific members of the Nima-Related Kinase (NEK) family have been linked to cancer development and progression, and a role for NEK5, one of the least studied members, in breast cancer has recently been proposed. However, while NEK5 is known to regulate centrosome separation and mitotic spindle assembly, NEK5 signalling mechanisms and function in this malignancy require further characterization. To this end, we established a model system featuring overexpression of NEK5 in the immortalized breast epithelial cell line MCF-10A. MCF-10A cells overexpressing NEK5 exhibited an increase in clonogenicity under monolayer conditions and enhanced acinar size and abnormal morphology in 3D Matrigel culture. Interestingly, they also exhibited a marked reduction in Src activation and downstream signalling. To interrogate NEK5 signalling and function in an unbiased manner, we applied a variety of MS-based proteomic approaches. Determination of the NEK5 interactome by Bio-ID identified a variety of protein classes including the kinesins KIF2C and KIF22, the mitochondrial proteins TFAM, TFB2M and MFN2, RhoH effectors and the negative regulator of Src, CSK. Characterization of proteins and phosphosites modulated upon NEK5 overexpression by global MS-based (phospho)proteomic profiling revealed impact on the cell cycle, DNA synthesis and repair, Rho GTPase signalling, the microtubule cytoskeleton and hemidesmosome assembly. Overall, the study indicates that NEK5 impacts diverse pathways and processes in breast epithelial cells, and likely plays a multifaceted role in breast cancer development and progression. Video Abstract.

Indexed as

Breast NeoplasmsProteomicsCell LineDNA-Binding ProteinsEpithelial CellsFemaleHumansKinesinsNIMA-Related KinasesDNA-Binding ProteinsKIF22 protein, humanKinesinsNEK5 protein, humanNIMA-Related KinasesBioiDBreast cancerKinaseNEK5NEKsProteomics

Identifiers

PMID36550548
PMCPMC9773587
OpenAlexW4312075316

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.