Evidence map›Paper›PMID 35022268›Full record

ArticleGut2022

CCT3-

Jonas Nørskov Søndergaard, Christian Sommerauer, Ionut Atanasoai, Laura C Hinte, Keyi Geng, Giulia Guiducci, Lars Bräutigam, Myriam Aouadi, Lovorka Stojic, Isabel Barragan and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  7. Chaperonin in health and disease.Molecular biomedicine · 2026
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  15. Translational cancer research · 2025
    Article
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  20. Review
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

11 authors at 3 institutions in 2 countries.

Jonas Nørskov SøndergaardDepartment of Microbiology, Tumor, and Cell Biology, Science for Life Laboratory, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-4438-6756
Christian SommerauerDepartment of Microbiology, Tumor, and Cell Biology, Science for Life Laboratory, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-7132-7172
Ionut AtanasoaiDepartment of Microbiology, Tumor, and Cell Biology, Science for Life Laboratory, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-0757-6681
Laura C HinteDepartment of Microbiology, Tumor, and Cell Biology, Science for Life Laboratory, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-4226-0009
Keyi GengDepartment of Microbiology, Tumor, and Cell Biology, Science for Life Laboratory, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-0892-7460
Giulia GuiducciBarts Cancer Institute, Centre for Cancer Cell and Molecular Biology, John Vane Science Centre, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0002-0632-6808
Lars BräutigamComparative Medicine, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-2834-1512
Myriam AouadiDepartment of Medicine, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-6256-7107
Lovorka StojicBarts Cancer Institute, Centre for Cancer Cell and Molecular Biology, John Vane Science Centre, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0001-6691-3396
Isabel BarraganDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-8586-6502
Claudia KutterDepartment of Microbiology, Tumor, and Cell Biology, Science for Life Laboratory, Karolinska Institute, Stockholm, Sweden claudia.kutter@ki.se.ORCID http://orcid.org/0000-0002-8047-0058
Science for Life Laboratory · SEKarolinska Institutet · SEQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo better comprehend transcriptional phenotypes of cancer cells, we globally characterised RNA-binding proteins (RBPs) to identify altered RNAs, including long non-coding RNAs (lncRNAs).

designTo unravel RBP-lncRNA interactions in cancer, we curated a list of ~2300 highly expressed RBPs in human cells, tested effects of RBPs and lncRNAs on patient survival in multiple cohorts, altered expression levels, integrated various sequencing, molecular and cell-based data.

resultsHigh expression of RBPs negatively affected patient survival in 21 cancer types, especially hepatocellular carcinoma (HCC). After knockdown of the top 10 upregulated RBPs and subsequent transcriptome analysis, we identified 88 differentially expressed lncRNAs, including 34 novel transcripts. CRISPRa-mediated overexpression of four lncRNAs had major effects on the HCC cell phenotype and transcriptome. Further investigation of four RBP-lncRNA pairs revealed involvement in distinct regulatory processes. The most noticeable RBP-lncRNA connection affected lipid metabolism, whereby the non-canonical RBP CCT3 regulated

conclusionsWe revealed that RBP gene expression is perturbed in HCC and identified that RBPs exerted additional functions beyond their tasks under normal physiological conditions, which can be stimulated or intensified via lncRNAs and affected tumour growth.

Indexed as

hepatocellular carcinomalipid metabolism

Identifiers

PMID35022268
PMCPMC9484377
OpenAlexW4206065980

What OpenQuestion 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 OpenQuestion graph.