Evidence map›Paper›PMID 35454801›Full record

ArticleCancers2022

Histone Demethylase KDM5C Drives Prostate Cancer Progression by Promoting EMT.

Anna-Lena Lemster, Elisabeth Sievers, Helen Pasternack, Pamela Lazar-Karsten, Niklas Klümper, Verena Sailer, Anne Offermann, Johannes Brägelmann, Sven Perner, Jutta Kirfel

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
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  6. Article
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  12. Article
  13. Article
  14. Epigenetic (De)regulation in Prostate Cancer.Cancer treatment and research · 2023
    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

10 authors at 3 institutions in 1 country.

Anna-Lena LemsterInstitute of Pathology, University Hospital Schleswig-Holstein, 23538 Luebeck, Germany.
Elisabeth SieversInstitute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.
Helen PasternackInstitute of Pathology, University Hospital Schleswig-Holstein, 23538 Luebeck, Germany.ORCID 0000-0003-2386-2300
Pamela Lazar-KarstenInstitute of Pathology, University Hospital Schleswig-Holstein, 23538 Luebeck, Germany.
Niklas KlümperDepartment of Urology and Pediatric Urology, University Hospital Bonn, 53127 Bonn, Germany.
Verena SailerInstitute of Pathology, University Hospital Schleswig-Holstein, 23538 Luebeck, Germany.
Anne OffermannInstitute of Pathology, University Hospital Schleswig-Holstein, 23538 Luebeck, Germany.
Johannes BrägelmannDepartment of Translational Genomics, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50931 Cologne, Germany.ORCID 0000-0002-1306-2169
Sven PernerInstitute of Pathology, University Hospital Schleswig-Holstein, 23538 Luebeck, Germany.
Jutta KirfelInstitute of Pathology, University Hospital Schleswig-Holstein, 23538 Luebeck, Germany.
University Hospital Schleswig-Holstein · DEUniversity Hospital Bonn · DEUniversity of Cologne · DE

Funding

DFG KI672/6-1Rudolf Becker Foundation TO321/36080/2020/kg
6 · The paper itself

Abstract

Prostate cancer (PCa) poses a major public health problem in men. Metastatic PCa is incurable, and ultimately threatens the life of many patients. Mutations in tumor suppressor genes and oncogenes are important for PCa progression, whereas the role of epigenetic factors in prostate carcinogenesis is insufficiently examined. The histone demethylase KDM5C exerts important roles in tumorigenesis. KDM5C has been reported to be highly expressed in various cancer cell types, particularly in primary PCa. Here, we could show that KDM5C is highly upregulated in metastatic PCa. Functionally, in KDM5C knockdown cells migratory and invasion capacity was reduced. Interestingly, modulation of KDM5C expression influences several EMT signaling pathways (e.g., Akt/mTOR), expression of EMT transcription factors, epigenetic modifiers, and miR-205, resulting in increased expression of E-cadherin and reduced expression of N-cadherin. Mouse xenografts of KDM5C knockdown cells showed reduced tumor growth. In addition, the Akt/mTOR pathway is one of the classic signaling pathways to mediate tumor metabolic homeostasis, which is beneficial for tumor growth and metastasis. Taken together, our findings indicate that a combination of a selective KDM5C- and Akt/mTOR-inhibitor might be a new promising therapeutic strategy to reduce metastatic burden in PCa.

Indexed as

CRPCepithelial-to-mesenchymal transitionhistone demethylaseKDM5Cprostate cancersignaling pathway

Identifiers

PMID35454801
PMCPMC9032772
OpenAlexW4224279140

What Socratic 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 Socratic graph.