Evidence map›Paper›PMID 34007958›Full record

ArticleiScience2021

Cytokeratin 5 determines maturation of the mammary myoepithelium.

Vivi Deckwirth, Eeva Kaisa Rajakylä, Sandhanakrishnan Cattavarayane, Anna Acheva, Niccole Schaible, Ramaswamy Krishnan, Juan José Valle-Delgado, Monika Österberg, Pia Björkenheim, Antti Sukura and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

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  6. Insights into the transition of ductal carcinomaCancer biology & medicine · 2022
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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

11 authors at 3 institutions in 2 countries.

Vivi DeckwirthSection of Pathology, Department of Veterinary Biosciences, University of Helsinki, Agnes Sjöberginkatu 2, Helsinki 00014, Finland.
Eeva Kaisa RajakyläSection of Pathology, Department of Veterinary Biosciences, University of Helsinki, Agnes Sjöberginkatu 2, Helsinki 00014, Finland.
Sandhanakrishnan CattavarayaneSection of Pathology, Department of Veterinary Biosciences, University of Helsinki, Agnes Sjöberginkatu 2, Helsinki 00014, Finland.
Anna AchevaSection of Pathology, Department of Veterinary Biosciences, University of Helsinki, Agnes Sjöberginkatu 2, Helsinki 00014, Finland.
Niccole SchaibleBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Ramaswamy KrishnanBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Juan José Valle-DelgadoDepartment of Bioproducts and Biosystems, School of Chemical Engineering, Aalto University, Espoo 00076, Finland.
Monika ÖsterbergDepartment of Bioproducts and Biosystems, School of Chemical Engineering, Aalto University, Espoo 00076, Finland.
Pia BjörkenheimVeterinary Teaching Hospital, University of Helsinki, Helsinki 00014, Finland.
Antti SukuraSection of Pathology, Department of Veterinary Biosciences, University of Helsinki, Agnes Sjöberginkatu 2, Helsinki 00014, Finland.
Sari TojkanderSection of Pathology, Department of Veterinary Biosciences, University of Helsinki, Agnes Sjöberginkatu 2, Helsinki 00014, Finland.
University of Helsinki · FIAalto University · FIBeth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At invasion, transformed mammary epithelial cells expand into the stroma through a disrupted myoepithelial (ME) cell layer and basement membrane (BM). The intact ME cell layer has thus been suggested to act as a barrier against invasion. Here, we investigate the mechanisms behind the disruption of ME cell layer. We show that the expression of basal/ME proteins CK5, CK14, and α-SMA altered along increasing grade of malignancy, and their loss affected the maintenance of organotypic 3D mammary architecture. Furthermore, our data suggests that loss of CK5 prior to invasive stage causes decreased levels of Zinc finger protein SNAI2 (SLUG), a key regulator of the mammary epithelial cell lineage determination. Consequently, a differentiation bias toward luminal epithelial cell type was detected with loss of mature, α-SMA-expressing ME cells and reduced deposition of basement membrane protein laminin-5. Therefore, our data discloses the central role of CK5 in mammary epithelial differentiation and maintenance of normal ME layer.

Indexed as

BiophysicsCell BiologyDevelopmental Biology

Identifiers

PMID34007958
PMCPMC8111680
OpenAlexW3154596646

What Socratic holds

Textmetadata
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 Socratic graph.