Evidence map›Paper›PMID 39613731›Full record

ArticleNature communications2024

KANK1 promotes breast cancer development by compromising Scribble-mediated Hippo activation.

Shiny Shengzhen Guo, Zhiying Liu, Guan M Wang, Zhiqi Sun, Kaikai Yu, James P Fawcett, Reinhard Buettner, Bo Gao, Reinhard Fässler

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Shiny Shengzhen GuoDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany. shguo@biochem.mpg.de.ORCID 0000-0001-9899-7491
Zhiying LiuSchool of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Guan M WangDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.ORCID 0000-0002-0390-6057
Zhiqi SunDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.ORCID 0000-0002-2792-2158
Kaikai YuDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
James P FawcettDepartments of Pharmacology and Surgery, Dalhousie University, Halifax, NS, B3H 4R2, Canada.
Reinhard BuettnerInstitute of Pathology, Medical Faculty, University Cologne, Cologne, Germany.ORCID 0000-0001-8806-4786
Bo GaoSchool of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0002-8684-5199
Reinhard FässlerDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.ORCID 0000-0002-0145-6937

Funding

EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)) 810104Gouvernement du Canada | Instituts de Recherche en Santé du Canada | CIHR Skin Research Training Centre (Skin Research Training Centre) 158738Gouvernement du Canada | Instituts de Recherche en Santé du Canada | CIHR Skin Research Training Centre (Skin Research Training Centre) 183923
6 · The paper itself

Abstract

KANK1 is expressed in epithelial cells and connects focal adhesions with the adjacent cortical microtubule stabilizing complex. Although KANK1 was shown to suppress cancer cell growth in vitro, TCGA database points to high KANK1 levels associated with poor prognosis in a wide spectrum of human malignancies. Here, we address this discrepancy and report that KANK1 promotes proliferation and survival of PyMT-transformed mammary tumor cells in vivo. Mechanistically, KANK1 localizes to the basal side of basement membrane (BM)-attached transformed luminal epithelial cells. When these cells lose the contact with the BM and disassemble integrin adhesions, KANK1 is found at cell-cell junctions where it competes with the polarity and tumor suppressor Scribble for NOS1AP binding, which curbs the ability of Scribble to promote Hippo pathway activity. The consequences are stabilization and nuclear accumulation of TAZ, growth and survival of tumor cells and elevated breast cancer development.

Indexed as

Adaptor Proteins, Signal TransducingBreast NeoplasmsCell ProliferationHippo Signaling PathwayProtein Serine-Threonine KinasesTumor Suppressor ProteinsAnimalsCell Line, TumorCytoskeletal ProteinsEpithelial CellsFemaleHumansIntercellular JunctionsIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceAdaptor Proteins, Signal TransducingCytoskeletal ProteinsIntracellular Signaling Peptides and ProteinsKANK1 protein, humanMembrane ProteinsProtein Serine-Threonine KinasesSCRIB protein, humanscrib protein, mouseTumor Suppressor ProteinsYAP-Signaling Proteins

Identifiers

PMID39613731
PMCPMC11607453

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Registered trials

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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.