Evidence map›Paper›PMID 33574609›Full record

ArticleNature biotechnology2021

A bacterial protease depletes c-MYC and increases survival in mouse models of bladder and colon cancer.

Daniel S C Butler, Caterina Cafaro, Johannes Putze, Murphy Lam Yim Wan, Thi Hien Tran, Ines Ambite, Shahram Ahmadi, Sven Kjellström, Charlotte Welinder, Sing Ming Chao and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature biotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

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  17. MYC-driven synthesis of Siglec ligands is a glycoimmune checkpoint.Proceedings of the National Academy of Sciences of the United States of America · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 3 countries.

Daniel S C Butler *Department of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-6717-545X
Caterina Cafaro *Department of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden.
Johannes PutzeInstitute of Hygiene, University of Münster, Münster, Germany.
Murphy Lam Yim WanDepartment of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden.
Thi Hien TranDepartment of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden.
Ines AmbiteDepartment of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0003-1470-671X
Shahram AhmadiDepartment of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden.
Sven KjellströmDepartment of Clinical Sciences, BioMS, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0003-4646-5279
Charlotte WelinderDepartment of Clinical Sciences, Division of Oncology and Pathology, Lund University, Lund, Sweden.
Sing Ming ChaoDepartment of Paediatrics, Nephrology Service, KK Women's and Children's Hospital, Singapore, Singapore.
Ulrich DobrindtInstitute of Hygiene, University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0001-9949-1898
Catharina SvanborgDepartment of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden. catharina.svanborg@med.lu.se.ORCID http://orcid.org/0000-0001-8145-0553
Lund University · SEUniversity of Münster · DEKK Women's and Children's Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Is the oncogene MYC upregulated or hyperactive? In the majority of human cancers, finding agents that target c-MYC has proved difficult. Here we report specific bacterial effector molecules that inhibit cellular MYC (c-MYC) in human cells. We show that uropathogenic Escherichia coli (UPEC) degrade the c-MYC protein and attenuate MYC expression in both human cells and animal tissues. c-MYC protein was rapidly degraded by both cell-free bacterial lysates and the purified bacterial protease Lon. In mice, intravesical or peroral delivery of Lon protease delayed tumor progression and increased survival in MYC-dependent bladder and colon cancer models, respectively. These results suggest that bacteria have evolved strategies to control c-MYC tissue levels in the host and that the Lon protease shows promise for therapeutic targeting of c-MYC in cancer.

Indexed as

Genes, mycAcute DiseaseAnimalsColonic NeoplasmsDisease Models, AnimalEscherichia coli InfectionsGene DeletionMiceNephritisUrinary Bladder NeoplasmsUropathogenic Escherichia coli

Identifiers

PMID33574609
OpenAlexW3127560017

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.