Evidence map›Paper›PMID 33082514›Full record

ArticleCell death and differentiation2021

The deubiquitinase JOSD2 is a positive regulator of glucose metabolism.

Lyudmila Krassikova, Boxi Zhang, Divya Nagarajan, André Lima Queiroz, Merve Kacal, Evangelos Samakidis, Helin Vakifahmetoglu-Norberg, Erik Norberg

Open access · greenAbstract read
In one paragraph

Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-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

29 citing papers in PubMed, 39 citations in OpenAlex.

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  12. Unveiling the Biological Function ofPlants (Basel, Switzerland) · 2024
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  16. Deubiquitinating enzyme JOSD2 affects susceptibility of non-small cell lung carcinoma cells to anti-cancer drugs through DNA damage repair.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    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

8 authors at 2 institutions in 2 countries.

Lyudmila Krassikova *Department of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden.
Boxi Zhang *Department of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden.
Divya NagarajanDepartment of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden.
André Lima QueirozDepartment of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden.
Merve KacalDepartment of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden.
Evangelos SamakidisDepartment of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden.
Helin Vakifahmetoglu-NorbergDepartment of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden.
Erik NorbergDepartment of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Solnavägen 9, SE-171 65, Stockholm, Sweden. Erik.Norberg@ki.se.
Karolinska Institutet · SECornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells undergo complex metabolic alterations. The mechanisms underlying the tuning of cancer metabolism are under active investigation. Here, we identify the uncharacterized deubiquitinase JOSD2 as a positive regulator of cancer cell proliferation by displaying comprehensive effects on glucose catabolism. We found that JOSD2 directly controls a metabolic enzyme complex that includes Aldolase A, Phosphofructokinase-1 and Phosphoglycerate dehydrogenase, in vitro and in vivo. Further, JOSD2 expression, but not a catalytically inactive mutant, deubiquitinates and stabilizes the enzyme complex, thereby enhancing their activities and the glycolytic rate. This represents a selective JOSD2 feature that is not shared among other Machado-Joseph disease DUBs or observed in nontransformed cells. JOSD2 deficiency displays cytostatic effects and reduces glycolysis in a broad spectrum of tumor cells of distinct origin and its expression correlates with poor prognosis in non-small cell lung cancer. Overall, our study provides evidence for a previously unknown biological mechanism in which JOSD2 integrates glucose and serine metabolism with potential therapeutic implications.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationEndopeptidasesFemaleFructose-Bisphosphate AldolaseGlucoseGlycolysisHumansLung NeoplasmsMiceMice, NudePhosphofructokinase-1Phosphoglycerate DehydrogenaseSerineEndopeptidasesFructose-Bisphosphate AldolaseGlucosePhosphofructokinase-1Phosphoglycerate DehydrogenaseSerine

Identifiers

PMID33082514
PMCPMC7937685
OpenAlexW3094277988

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.