Evidence map›Paper›PMID 33046706›Full record

ArticleNature communications2020

Cathepsin D deficiency in mammary epithelium transiently stalls breast cancer by interference with mTORC1 signaling.

Stephanie Ketterer, Julia Mitschke, Anett Ketscher, Manuel Schlimpert, Wilfried Reichardt, Natascha Baeuerle, Maria Elena Hess, Patrick Metzger, Melanie Boerries, Christoph Peters and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  20. Theranostics · 2025
    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

14 authors at 2 institutions in 1 country.

Stephanie KettererInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.
Julia MitschkeInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.
Anett KetscherInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.
Manuel SchlimpertFaculty of Biology, University of Freiburg, Freiburg, 79104, Germany.
Wilfried ReichardtGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), partner site Freiburg, Freiburg, 79104, Germany.ORCID http://orcid.org/0000-0002-8888-399X
Natascha BaeuerleInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.
Maria Elena HessInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.
Patrick MetzgerInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.ORCID http://orcid.org/0000-0002-2451-1943
Melanie BoerriesInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.ORCID http://orcid.org/0000-0002-3670-0602
Christoph PetersInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.
Bernd KammererCentre for Integrative Signalling Analysis (CISA), University of Freiburg, Freiburg, 79104, Germany.
Tilman BrummerInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany.ORCID http://orcid.org/0000-0003-4387-7905
Florian SteinbergCentre for Integrative Signalling Analysis (CISA), University of Freiburg, Freiburg, 79104, Germany.
Thomas ReinheckelInstitute of Molecular Medicine and Cell Research, University of Freiburg, Freiburg, 79104, Germany. thomas.reinheckel@mol-med.uni-freiburg.de.ORCID http://orcid.org/0000-0001-9866-9105
University of Freiburg · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cathepsin D (CTSD) is a lysosomal protease and a marker of poor prognosis in breast cancer. However, the cells responsible for this association and the function of CTSD in cancer are still incompletely understood. By using a conditional CTSD knockout mouse crossed to the transgenic MMTV-PyMT breast cancer model we demonstrate that CTSD deficiency in the mammary epithelium, but not in myeloid cells, blocked tumor development in a cell-autonomous manner. We show that lack of CTSD impaired mechanistic Target of Rapamycin Complex 1 (mTORC1) signaling and induced reversible cellular quiescence. In line, CTSD-deficient tumors started to grow with a two-month delay and quiescent Ctsd

Indexed as

AnimalsBreast NeoplasmsCathepsin DEpitheliumFemaleHumansMammary Glands, AnimalMechanistic Target of Rapamycin Complex 1Mice, Inbred BALB CMice, Inbred C57BLMice, KnockoutSignal TransductionCathepsin DCtsd protein, mouseMechanistic Target of Rapamycin Complex 1

Identifiers

PMID33046706
PMCPMC7552405
OpenAlexW3092177313

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.