Evidence map›Paper›PMID 30903103›Full record

ArticleCell death and differentiation2019

FGFR4 phosphorylates MST1 to confer breast cancer cells resistance to MST1/2-dependent apoptosis.

S Pauliina Turunen, Pernilla von Nandelstadh, Tiina Öhman, Erika Gucciardo, Brinton Seashore-Ludlow, Beatriz Martins, Ville Rantanen, Huini Li, Katrin Höpfner, Päivi Östling and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 63 citations in OpenAlex.

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  11. Genes & diseases · 2024
    Article
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  13. Article
  14. Review
  15. Article
  16. Targeting Breast Cancer Stem Cells.International journal of biological sciences · 2023
    Review
  17. Article
  18. Article
  19. Theranostics · 2022
    Article
  20. 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

12 authors at 4 institutions in 2 countries.

S Pauliina Turunen *Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, SE-171 77, Sweden.
Pernilla von Nandelstadh *Research Programs Unit, Genome-Scale Biology, Medicum, University of Helsinki and Helsinki University Hospital, Helsinki, FI-00014, Finland.
Tiina ÖhmanInstitute of Biotechnology, Helsinki Institute of Life Science, University of Helsinki, Helsinki, FI-00014, Finland.
Erika GucciardoResearch Programs Unit, Genome-Scale Biology, Medicum, University of Helsinki and Helsinki University Hospital, Helsinki, FI-00014, Finland.
Brinton Seashore-LudlowDepartment of Oncology and Pathology, Science for Life Laboratory, Karolinska Institutet, Stockholm, SE-171 77, Sweden.
Beatriz MartinsResearch Programs Unit, Genome-Scale Biology, Medicum, University of Helsinki and Helsinki University Hospital, Helsinki, FI-00014, Finland.
Ville RantanenResearch Programs Unit, Genome-Scale Biology, Medicum, University of Helsinki and Helsinki University Hospital, Helsinki, FI-00014, Finland.
Huini LiDepartment of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, SE-171 77, Sweden.
Katrin HöpfnerResearch Programs Unit, Genome-Scale Biology, Medicum, University of Helsinki and Helsinki University Hospital, Helsinki, FI-00014, Finland.
Päivi ÖstlingDepartment of Oncology and Pathology, Science for Life Laboratory, Karolinska Institutet, Stockholm, SE-171 77, Sweden.
Markku VarjosaloInstitute of Biotechnology, Helsinki Institute of Life Science, University of Helsinki, Helsinki, FI-00014, Finland.
Kaisa LehtiDepartment of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, SE-171 77, Sweden. kaisa.lehti@ki.se.
University of Helsinki · FIHelsinki University Hospital · FIKarolinska Institutet · SEScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells balance with the equilibrium of cell death and growth to expand and metastasize. The activity of mammalian sterile20-like kinases (MST1/2) has been linked to apoptosis and tumor suppression via YAP/Hippo pathway-independent and -dependent mechanisms. Using a kinase substrate screen, we identified here MST1 and MST2 among the top substrates for fibroblast growth factor receptor 4 (FGFR4). In COS-1 cells, MST1 was phosphorylated at Y433 residue in an FGFR4 kinase activity-dependent manner, as assessed by mass spectrometry. Blockade of this phosphorylation by Y433F mutation induced MST1 activation, as indicated by increased threonine phosphorylation of MST1/2, and the downstream substrate MOB1, in FGFR4-overexpressing T47D and MDA-MB-231 breast cancer cells. Importantly, the specific knockdown or short-term inhibition of FGFR4 in endogenous models of human HER2

Indexed as

AnimalsApoptosisBreast NeoplasmsCell Line, TumorChlorocebus aethiopsCOS CellsFemaleHippo KinasesHumansIntracellular Signaling Peptides and ProteinsMCF-7 CellsPhosphorylationProtein Serine-Threonine KinasesReceptor, Fibroblast Growth Factor, Type 4Serine-Threonine Kinase 3TransfectionFGFR4 protein, humanHippo KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesReceptor, Fibroblast Growth Factor, Type 4Serine-Threonine Kinase 3STK3 protein, humanSTK4 protein, human

Identifiers

PMID30903103
PMCPMC7224384
OpenAlexW2949159574

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.