Evidence map›Paper›PMID 29886796›Full record

ReviewCell cycle (Georgetown, Tex.)2018

Mitostemness.

Elisabet Cuyàs, Sara Verdura, Núria Folguera-Blasco, Cristian Bastidas-Velez, Ángel G Martin, Tomás Alarcón, Javier A Menendez

Abstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Cancer Stem Cell Metabolism.Advances in experimental medicine and biology · 2021
    Article
  9. Review
  10. Mitochondria in cancer.Cell stress · 2020
    Review
  11. Article
  12. Article
  13. A Shifty Target: Tumor-Initiating Cells and Their Metabolism.International journal of molecular sciences · 2019
    Review
  14. Article
  15. Article
  16. Mitochondrial dynamics and metastasis.Cellular and molecular life sciences : CMLS · 2019
    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

7 authors.

Elisabet Cuyàsa Program Against Cancer Therapeutic Resistance (ProCURE), Metabolism and Cancer Group , Catalan Institute of Oncology , Girona , Spain.ORCID 0000-0001-5353-440X
Sara Verduraa Program Against Cancer Therapeutic Resistance (ProCURE), Metabolism and Cancer Group , Catalan Institute of Oncology , Girona , Spain.ORCID 0000-0001-8980-0423
Núria Folguera-Blascoc Centre de Recerca Matemàtica , Barcelona , Spain.ORCID 0000-0003-1584-5885
Cristian Bastidas-Velezb Girona Biomedical Research Institute (IDIBGI) , Girona , Spain.ORCID 0000-0003-2279-9266
Ángel G Martind StemTek Therapeutics , Bilbao , Spain.
Tomás Alarcónc Centre de Recerca Matemàtica , Barcelona , Spain.
Javier A Menendeza Program Against Cancer Therapeutic Resistance (ProCURE), Metabolism and Cancer Group , Catalan Institute of Oncology , Girona , Spain.ORCID 0000-0001-8733-4561

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unraveling the key mechanisms governing the retention versus loss of the cancer stem cell (CSC) state would open new therapeutic avenues to eradicate cancer. Mitochondria are increasingly recognized key drivers in the origin and development of CSC functional traits. We here propose the new term "mitostemness" to designate the mitochondria-dependent signaling functions that, evolutionary rooted in the bacterial origin of mitochondria, regulate the maintenance of CSC self-renewal and resistance to differentiation. Mitostemness traits, namely mitonuclear communication, mitoproteome components, and mitochondrial fission/fusion dynamics, can be therapeutically exploited to target the CSC state. We briefly review the pre-clinical evidence of action of investigational compounds on mitostemness traits and discuss ongoing strategies to accelerate the clinical translation of new mitostemness drugs. The recognition that the bacterial origin of present-day mitochondria can drive decision-making signaling phenomena may open up a new therapeutic dimension against life-threatening CSCs. New therapeutics aimed to target mitochondria not only as biochemical but also as biophysical and morpho-physiological hallmarks of CSC might certainly guide improvements to cancer treatment.

Indexed as

Antineoplastic AgentsBacteriaCell NucleusHumansMitochondriaMitochondrial DynamicsNeoplastic Stem CellsAntineoplastic AgentsCancer stem cellsmetabolismmitochondria

Identifiers

PMID29886796
PMCPMC6103691

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.