Evidence map›Paper›PMID 39468273›Full record

ArticleScientific reports2024

Loss of myosin light chain kinase induces the cellular senescence associated secretory phenotype to promote breast epithelial cell migration.

Dayoung Kim, Jonathan A Cooper, David M Helfman

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
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

3 authors.

Dayoung KimBasic Sciences Division, Fred Hutchinson Cancer Center, Seattle, WA, 98109, USA. dkim23@fredhutch.org.
Jonathan A CooperBasic Sciences Division, Fred Hutchinson Cancer Center, Seattle, WA, 98109, USA.
David M HelfmanDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.

Funding

National Research Foundation of Korea NFR 2018R1A2A2A05021262
6 · The paper itself

Abstract

Overexpression or activation of oncogenes or loss of tumor-suppressor genes can induce cellular senescence as a defense mechanism against tumor development, thereby maintaining cellular homeostasis. However, cancer cells can circumvent this senescent state and continue to spread. Myosin light chain kinase (MLCK) is downregulated in many breast cancers. Here we report that downregulation of MLCK in normal breast epithelial cells induces a senescence-associated secretory phenotype and stimulates migration. The reduction of MLCK results in increased p21

Indexed as

Cell MovementCyclin-Dependent Kinase Inhibitor p21Epithelial CellsMyosin-Light-Chain KinaseBreastBreast NeoplasmsCalcium-Binding ProteinsCellular SenescenceFemaleHumansIntercellular Adhesion Molecule-1Proto-Oncogene Proteins c-aktSenescence-Associated Secretory PhenotypeSignal TransductionTOR Serine-Threonine KinasesTumor Suppressor Protein p53Calcium-Binding ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Intercellular Adhesion Molecule-1MTOR protein, humanMYLK protein, humanMyosin-Light-Chain KinaseProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTumor Suppressor Protein p53Breast cancerCell migrationMTORMyosin light chain kinaseP21Senescence-associated secretory phenotype

Identifiers

PMID39468273
PMCPMC11519378

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.