Evidence map›Paper›PMID 34503213›Full record

ReviewCancers2021

Therapeutic Potential of Targeting the SUMO Pathway in Cancer.

Antti Kukkula, Veera K Ojala, Lourdes M Mendez, Lea Sistonen, Klaus Elenius, Maria Sundvall

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 94 citations in OpenAlex.

  1. A RAC1 SUMOylation switch governs breast cancer metastasis.Signal transduction and targeted therapy · 2026
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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 3 institutions in 2 countries.

Antti KukkulaCancer Research Unit, FICAN West Cancer Center Laboratory, Institute of Biomedicine, Turku University Hospital, University of Turku, FI-20520 Turku, Finland.
Veera K OjalaCancer Research Unit, FICAN West Cancer Center Laboratory, Institute of Biomedicine, Turku University Hospital, University of Turku, FI-20520 Turku, Finland.
Lourdes M MendezBeth Israel Deaconess Cancer Center, Beth Israel Deaconess Medical Center, Department of Medicine and Pathology, Cancer Research Institute, Harvard Medical School, Boston, MA 02115, USA.
Lea SistonenTurku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520 Turku, Finland.
Klaus EleniusCancer Research Unit, FICAN West Cancer Center Laboratory, Institute of Biomedicine, Turku University Hospital, University of Turku, FI-20520 Turku, Finland.ORCID 0000-0001-5700-0827
Maria SundvallCancer Research Unit, FICAN West Cancer Center Laboratory, Institute of Biomedicine, Turku University Hospital, University of Turku, FI-20520 Turku, Finland.
Åbo Akademi University · FIUniversity of Turku · FIBeth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SUMOylation is a dynamic and reversible post-translational modification, characterized more than 20 years ago, that regulates protein function at multiple levels. Key oncoproteins and tumor suppressors are SUMO substrates. In addition to alterations in SUMO pathway activity due to conditions typically present in cancer, such as hypoxia, the SUMO machinery components are deregulated at the genomic level in cancer. The delicate balance between SUMOylation and deSUMOylation is regulated by SENP enzymes possessing SUMO-deconjugation activity. Dysregulation of SUMO machinery components can disrupt the balance of SUMOylation, contributing to the tumorigenesis and drug resistance of various cancers in a context-dependent manner. Many molecular mechanisms relevant to the pathogenesis of specific cancers involve SUMO, highlighting the potential relevance of SUMO machinery components as therapeutic targets. Recent advances in the development of inhibitors targeting SUMOylation and deSUMOylation permit evaluation of the therapeutic potential of targeting the SUMO pathway in cancer. Finally, the first drug inhibiting SUMO pathway, TAK-981, is currently also being evaluated in clinical trials in cancer patients. Intriguingly, the inhibition of SUMOylation may also have the potential to activate the anti-tumor immune response. Here, we comprehensively and systematically review the recent developments in understanding the role of SUMOylation in cancer and specifically focus on elaborating the scientific rationale of targeting the SUMO pathway in different cancers.

Indexed as

cancerpost-translational modification (PTM)protein inhibitor of activated STAT (PIAS)sentrin-specific protease (SENP)small ubiquitin-like modifier (SUMO)

Identifiers

PMID34503213
PMCPMC8431684
OpenAlexW3197902239

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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 OpenQuestion graph.