Evidence map›Paper›PMID 25957406›Full record

ArticleThe Journal of biological chemistry2015

Stress-resistant Translation of Cathepsin L mRNA in Breast Cancer Progression.

Martina Tholen, Julia Wolanski, Britta Stolze, Marco Chiabudini, Mieczyslaw Gajda, Peter Bronsert, Elmar Stickeler, Sabine Rospert, Thomas Reinheckel

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Martina TholenInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; Faculty of Biology, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany.
Julia WolanskiInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany.
Britta StolzeInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany.
Marco ChiabudiniInstitute of Biochemistry and Molecular Biology, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-University Freiburg, 79104 Freiburg.
Mieczyslaw GajdaInstitute of Pathology, Friedrich-Schiller University, 07743 Jena, Germany.
Peter BronsertInstitute of Pathology, University Medical Center Freiburg, 79106 Freiburg; Comprehensive Cancer Center/German Cancer Consortium (DKTK), 79106 Freiburg.
Elmar StickelerComprehensive Cancer Center/German Cancer Consortium (DKTK), 79106 Freiburg; Clinic for Gynecology, University Medical Center Freiburg, 79106 Freiburg, Germany.
Sabine RospertInstitute of Biochemistry and Molecular Biology, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-University Freiburg, 79104 Freiburg.
Thomas ReinheckelInstitute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-University Freiburg, 79104 Freiburg; Comprehensive Cancer Center/German Cancer Consortium (DKTK), 79106 Freiburg. Electronic address: thomas.reinheckel@uniklinik-freiburg.de.
University of Freiburg · DEDeutschen Konsortium für Translationale Krebsforschung · DEFriedrich Schiller University Jena · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cysteine protease cathepsin L (CTSL) is often thought to act as a tumor promoter by enhancing tumor progression and metastasis. This goes along with increased CTSL activity in various tumor entities; however, the mechanisms leading to high CTSL levels are incompletely understood. With the help of the polyoma middle T oncogene driven breast cancer mouse model expressing a human CTSL genomic transgene, we show that CTSL indeed promotes breast cancer metastasis to the lung. During tumor formation and progression high expression levels of CTSL are maintained by enduring translation of CTSL mRNA. Interestingly, human breast cancer specimens expressed the same pattern of 5' untranslated region (UTR) splice variants as the transgenic mice and the human cancer cell line MDA-MB 321. By polyribosome profiling of tumor tissues and human breast cancer cells, we observe an intrinsic resistance of CTSL to stress-induced shutdown of translation. This ability can be attributed to all 5' UTR variants of CTSL and is not dependent on a previously described internal ribosomal entry site motif. In conclusion, we provide in vivo functional evidence for overexpressed CTSL as a promoter of lung metastasis, whereas high CTSL levels are maintained during tumor progression due to stress-resistant mRNA translation.

Indexed as

5' Untranslated RegionsProtein BiosynthesisStress, PhysiologicalAnimalsBreast NeoplasmsCathepsin LCell Line, TumorFemaleHumansLung NeoplasmsMammary Neoplasms, ExperimentalMiceMice, TransgenicNeoplasm MetastasisRNA, Neoplasm5' Untranslated RegionsCathepsin LCTSL protein, humanCtsl protein, mouseRNA, Neoplasmalternative splicingbreast cancercysteine proteasemetastasistranslation control

Identifiers

PMID25957406
PMCPMC4505485
OpenAlexW281330656

What OpenQuestion holds

Textmetadata
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.