Evidence map›Paper›PMID 35189384›Full record

ArticleMitochondrion2022

Cancer/Testis Antigen 55 is required for cancer cell proliferation and mitochondrial DNA maintenance.

Jade Aurrière, David Goudenege, Simone A Baechler, Shar-Yin N Huang, Naig Gueguen, Valerie Desquiret-Dumas, Floris Chabrun, Rodolphe Perrot, Arnaud Chevrollier, Majida Charif and 4 more

Open access · greenAbstract read
In one paragraph

Article in Mitochondrion, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 50% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
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

14 authors at 5 institutions in 2 countries.

Jade AurrièreMitoLab Team, MitoVasc Unit, CNRS UMR6015, INSERM U1083, SFR ICAT, Angers University, Angers, France.
David GoudenegeMitoLab Team, Institut MitoVasc, CNRS UMR6015, INSERM U1083, Angers University, Angers, France; Departments of Biochemistry and Genetics, University Hospital Angers, Angers, France.
Simone A BaechlerLaboratory of Molecular Pharmacology, Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Shar-Yin N HuangLaboratory of Molecular Pharmacology, Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Naig GueguenMitoLab Team, Institut MitoVasc, CNRS UMR6015, INSERM U1083, Angers University, Angers, France; Departments of Biochemistry and Genetics, University Hospital Angers, Angers, France.
Valerie Desquiret-DumasMitoLab Team, Institut MitoVasc, CNRS UMR6015, INSERM U1083, Angers University, Angers, France; Departments of Biochemistry and Genetics, University Hospital Angers, Angers, France.
Floris ChabrunMitoLab Team, Institut MitoVasc, CNRS UMR6015, INSERM U1083, Angers University, Angers, France; Departments of Biochemistry and Genetics, University Hospital Angers, Angers, France.
Rodolphe PerrotSCIAM, Institut de Biologie en Sante, Angers University, Angers 49933, France.
Arnaud ChevrollierMitoLab Team, MitoVasc Unit, CNRS UMR6015, INSERM U1083, SFR ICAT, Angers University, Angers, France.
Majida CharifMitoLab Team, MitoVasc Unit, CNRS UMR6015, INSERM U1083, SFR ICAT, Angers University, Angers, France.
Olivier R BarisMitoLab Team, MitoVasc Unit, CNRS UMR6015, INSERM U1083, SFR ICAT, Angers University, Angers, France.
Yves PommierLaboratory of Molecular Pharmacology, Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Guy LenaersMitoLab Team, MitoVasc Unit, CNRS UMR6015, INSERM U1083, SFR ICAT, Angers University, Angers, France.
Salim KhiatiMitoLab Team, MitoVasc Unit, CNRS UMR6015, INSERM U1083, SFR ICAT, Angers University, Angers, France. Electronic address: salim.khiati@univ-angers.fr.
Centre National de la Recherche Scientifique · FRInserm · FRUniversité d'Angers · FRNational Cancer Institute · USCenter for Cancer Research · US

Funding

DNA Repair, Cell Cycle Checkpoints and Apoptosis as Targets for Anticancer DrugsZIABC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$23.0M
DNA Topoisomerases as Target of Action of Anticancer DrugsZIABC006161 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$16.8M
PROTEIN-ASSOCIATED DNA BREAKS AS INDICATOR OF TOPOISOMERASE INHIBITIONZ01BC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 1996 to 2008
$1.5M
Intramural NIH HHS Z01 BC006150Intramural NIH HHS ZIA BC006161
6 · The paper itself

Abstract

Cancer/Testis Antigens (CTAs) represent a group of proteins whose expression under physiological conditions is restricted to testis but activated in many human cancers. Also, it was observed that co-expression of multiple CTAs worsens the patient prognosis. Five CTAs were reported acting in mitochondria and we recently reported 147 transcripts encoded by 67 CTAs encoding for proteins potentially targeted to mitochondria. Among them, we identified the two isoforms encoded by CT55 for whom the function is poorly understood. First, we found that patients with tumors expressing wild-type CT55 are associated with poor survival. Moreover, CT55 silencing decreases dramatically cell proliferation. Second, to investigate the role of CT55 on mitochondria, we first show that CT55 is localized to both mitochondria and endoplasmic reticulum (ER) due to the presence of an ambiguous N-terminal targeting signal. Then, we show that CT55 silencing decreases mtDNA copy number and delays mtDNA recovery after an acute depletion. Moreover, demethylation of CT55 promotor increases its expression, which in turn increases mtDNA copy number. Finally, we measured the mtDNA copy number in NCI-60 cell lines and screened for genes whose expression is strongly correlated to mtDNA amount. We identified CT55 as the second highest correlated hit. Also, we show that compared to siRNA scrambled control (siCtrl) treatment, CT55 specific siRNA (siCT55) treatment down-regulates aerobic respiration, indicating that CT55 sustains mitochondrial respiration. Altogether, these data show for first time that CT55 acts on mtDNA copy number, modulates mitochondrial activity to sustain cancer cell proliferation.

Indexed as

DNA, MitochondrialNeoplasmsCell ProliferationDNA Copy Number VariationsHumansMaleMitochondriaRNA, Small InterferingTestisDNA, MitochondrialRNA, Small InterferingCell proliferationCT55Mitochondrial DNANCI-60

Identifiers

PMID35189384
PMCPMC9057655
OpenAlexW4213093374

What OpenQuestion holds

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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.