Evidence mapPaperPMID 34209043Full record

ArticleCancers2021

Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase.

Federica Pierucci, Alessia Frati, Chiara Battistini, Fabio Penna, Paola Costelli, Elisabetta Meacci

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. 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 15% 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. Review
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  3. Article
  4. Article
  5. Article
  6. Potential Vitamin E Signaling Mediators in Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2024
    Review
  7. Article
  8. Review
  9. Review
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  12. Article
  13. Article
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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

6 authors at 2 institutions in 1 country.

Federica PierucciDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio"-Unit of Biochemical Sciences and Molecular Biology, University of Florence, Viale GB Morgagni 50, 50134 Florence, Italy.ORCID 0000-0003-0196-8112
Alessia FratiDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio"-Unit of Biochemical Sciences and Molecular Biology, University of Florence, Viale GB Morgagni 50, 50134 Florence, Italy.
Chiara BattistiniDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio"-Unit of Biochemical Sciences and Molecular Biology, University of Florence, Viale GB Morgagni 50, 50134 Florence, Italy.
Fabio PennaDepartment of Clinical and Biological Sciences, University of Turin, 10125 Torino, Italy.ORCID 0000-0002-2774-6027
Paola CostelliDepartment of Clinical and Biological Sciences, University of Turin, 10125 Torino, Italy.
Elisabetta MeacciDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio"-Unit of Biochemical Sciences and Molecular Biology, University of Florence, Viale GB Morgagni 50, 50134 Florence, Italy.ORCID 0000-0002-5820-7800
University of Florence · ITUniversity of Turin · IT

Funding

Fondazione Banche di Pistoia e Vignole 2011Ministero dell'Istruzione, dell'Università e della Ricerca 2019-17
6 · The paper itself

Abstract

Apart from cytokines and chemokines, sphingolipid mediators, particularly sphingosine-1-phosphate (S1P) and ceramide 1-phosphate (C1P), contribute to cancer and inflammation. Cancer, as well as other inflammatory conditions, are associated with skeletal muscle (SkM) atrophy, which is characterized by the unbalance between protein synthesis and degradation. Although the signaling pathways involved in SkM mass wasting are multiple, the regulatory role of simple sphingolipids is limited. Here, we report the impairment of ceramide kinase (CerK), the enzyme responsible for the phosphorylation of ceramide to C1P, associated with the accomplishment of atrophic phenotype in various experimental models of SkM atrophy: in vivo animal model bearing the C26 adenocarcinoma or Lewis lung carcinoma tumors, in human and murine SkM cells treated with the conditioned medium obtained from cancer cells or with the glucocorticoid dexamethasone. Notably, we demonstrate in all the three experimental approaches a drastic decrease of CerK expression. Gene silencing of CerK promotes the up-regulation of atrogin-1/MAFbx expression, which was also observed after cell treatment with C8-ceramide, a biologically active ceramide analogue. Conversely, C1P treatment significantly reduced the corticosteroid's effects. Altogether, these findings provide evidence that CerK, acting as a molecular modulator, may be a new possible target for SkM mass regulation associated with cancer or corticosteroids.

Indexed as

atrogin-1/MAFbxC2C12 skeletal muscle cellscachexiaceramideceramide kinaseglucocorticoidsskeletal muscle mass wastingsphingolipids

Identifiers

PMID34209043
PMCPMC8269416
OpenAlexW3176202534

What Socratic holds

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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.