Evidence map›Paper›PMID 30850580›Full record

ArticleOncogenesis2019

Human colon cancer cells highly express myoferlin to maintain a fit mitochondrial network and escape p53-driven apoptosis.

Gilles Rademaker, Brunella Costanza, Justine Bellier, Michael Herfs, Raphaël Peiffer, Ferman Agirman, Naïma Maloujahmoum, Yvette Habraken, Philippe Delvenne, Akeila Bellahcène and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  7. Neoexpression ofJournal of personalized medicine · 2022
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  14. BRAFOncogene · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Gilles RademakerMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.
Brunella CostanzaMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.
Justine BellierMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.
Michael HerfsLaboratory of Experimental Pathology, GIGA Cancer, University of Liège, Liège, Belgium.
Raphaël PeifferMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.
Ferman AgirmanMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.
Naïma MaloujahmoumMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.
Yvette HabrakenLaboratory of Virology and Immunology, GIGA Molecular Biology of Disease, University of Liège, Liège, Belgium.
Philippe DelvenneLaboratory of Experimental Pathology, GIGA Cancer, University of Liège, Liège, Belgium.
Akeila BellahcèneMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.
Vincent CastronovoMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium.ORCID http://orcid.org/0000-0003-2351-6272
Olivier PeulenMetastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium. olivier.peulen@uliege.be.ORCID http://orcid.org/0000-0002-6933-0134
University of Liège · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon adenocarcinoma is the third most commonly diagnosed cancer and the second deadliest one. Metabolic reprogramming, described as an emerging hallmark of malignant cells, includes the predominant use of glycolysis to produce energy. Recent studies demonstrated that mitochondrial electron transport chain inhibitor reduced colon cancer tumour growth. Accumulating evidence show that myoferlin, a member of the ferlin family, is highly expressed in several cancer types, where it acts as a tumour promoter and participates in the metabolic rewiring towards oxidative metabolism. In this study, we showed that myoferlin expression in colon cancer lesions is associated with low patient survival and is higher than in non-tumoural adjacent tissue. Human colon cancer cells silenced for myoferlin exhibit a reduced oxidative phosphorylation activity associated with mitochondrial fission leading, ROS accumulation, decreased cell growth, and increased apoptosis. We observed the triggering of a DNA damage response culminating to a cell cycle arrest in wild-type p53 cells. The use of a p53 null cell line or a compound able to restore p53 activity (Prima-1) reverted the effects induced by myoferlin silencing, confirming the involvement of p53. The recent identification of a compound interacting with a myoferlin C2 domain and bearing anticancer potency identifies, together with our demonstration, this protein as a suitable new therapeutic target in colon cancer.

Identifiers

PMID30850580
PMCPMC6408501
OpenAlexW2922140127

What OpenQuestion holds

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Registered trials

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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.