Evidence mapPaperPMID 36732018Full record

ArticleLife science alliance2023

Loss of dyskerin facilitates the acquisition of metastatic traits by altering the mevalonate pathway.

Evelyn Andrades, Agustí Toll, Gustavo Deza, Sonia Segura, Ramón Gimeno, Guadalupe Espadas, Eduard Sabidó, Noemí Haro, Óscar J Pozo, Marta Bódalo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

13 authors at 4 institutions in 1 country.

Evelyn AndradesGroup of Inflammatory and Neoplastic Dermatological Diseases, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.ORCID https://orcid.org/0000-0003-2166-6760
Agustí TollGroup of Inflammatory and Neoplastic Dermatological Diseases, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.ORCID https://orcid.org/0000-0003-2656-0076
Gustavo DezaDepartment of Dermatology, Hospital del Mar, Parc de Salut Mar, Barcelona, Spain.ORCID https://orcid.org/0000-0001-8641-5327
Sonia SeguraDepartment of Dermatology, Hospital del Mar, Parc de Salut Mar, Barcelona, Spain.ORCID https://orcid.org/0000-0003-0653-1382
Ramón GimenoLaboratory of Immunology, Department of Pathology, Hospital del Mar, Parc de Salut Mar, Barcelona, Spain.ORCID https://orcid.org/0000-0002-8758-121X
Guadalupe EspadasProteomics Unit, Centre de Regulació Genòmica, Barcelona Institute of Science and Technology, Barcelona, Spain.ORCID https://orcid.org/0000-0002-6415-8013
Eduard SabidóProteomics Unit, Centre de Regulació Genòmica, Barcelona Institute of Science and Technology, Barcelona, Spain.ORCID https://orcid.org/0000-0001-6506-7714
Noemí HaroApplied Metabolomics Research Group, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.ORCID https://orcid.org/0000-0003-0604-770X
Óscar J PozoApplied Metabolomics Research Group, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.ORCID https://orcid.org/0000-0002-1735-9728
Marta BódaloMARGenomics, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.ORCID https://orcid.org/0000-0002-5950-4700
Paloma TorresGroup of Inflammatory and Neoplastic Dermatological Diseases, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.
Ramon M PujolDepartment of Dermatology, Hospital del Mar, Parc de Salut Mar, Barcelona, Spain.ORCID https://orcid.org/0000-0002-5622-6055
Inmaculada Hernández-MuñozGroup of Inflammatory and Neoplastic Dermatological Diseases, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain mhernandez@imim.es.ORCID https://orcid.org/0000-0003-3436-9634
Hospital Del Mar · ESParc de Salut · ESUniversitat Pompeu Fabra · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The initial dissemination of cancer cells from many primary tumors implies intravasation to lymphatic nodes or blood vessels. To investigate the mechanisms involved, we analyzed the expression of small non-coding RNAs in cutaneous squamous cell carcinoma (cSCC), a prevalent tumor that mainly spreads to lymph nodes. We report the reduced expression of small nucleolar RNAs in primary cSCCs that metastasized when compared to non-metastasizing cSCCs, and the progressive loss of DKC1 (dyskerin, which stabilizes the small nucleolar RNAs) along the metastasis. DKC1 depletion in cSCC cells triggered lipid metabolism by altering the mevalonate pathway and the acquisition of metastatic traits. Treatment of DKC1-depleted cells with simvastatin, an inhibitor of the mevalonate pathway, blocked the expression of proteins involved in the epithelial-to-mesenchymal transition. Consistently, the expression of the enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 1 was associated with pathological features of high metastatic risk in cSCC patients. Our data underpin the relevance of the mevalonate metabolism in metastatic dissemination and pave the possible incorporation of therapeutic approaches among the antineoplastic drugs used in routine patient care.

Indexed as

Carcinoma, Squamous CellSkin NeoplasmsCell Cycle ProteinsHumansMevalonic AcidNuclear ProteinsPhenotypeSimvastatinCell Cycle ProteinsDKC1 protein, humanMevalonic AcidNuclear ProteinsSimvastatin

Identifiers

PMID36732018
PMCPMC9899484
OpenAlexW4318976390

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.