Evidence map›Paper›PMID 24632851›Full record

ArticlePloS one2014

Persistent mitochondrial hyperfusion promotes G2/M accumulation and caspase-dependent cell death.

Laura M Westrate, Aaron D Sayfie, Danielle M Burgenske, Jeffrey P MacKeigan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Depletion ofFrontiers in molecular biosciences · 2022
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Laura M WestrateLaboratory of Systems Biology, Van Andel Research Institute, Grand Rapids, Michigan, United States of America; Van Andel Institute Graduate School, Grand Rapids, Michigan, United States of America.
Aaron D SayfieLaboratory of Systems Biology, Van Andel Research Institute, Grand Rapids, Michigan, United States of America.
Danielle M BurgenskeLaboratory of Systems Biology, Van Andel Research Institute, Grand Rapids, Michigan, United States of America; Van Andel Institute Graduate School, Grand Rapids, Michigan, United States of America.
Jeffrey P MacKeiganLaboratory of Systems Biology, Van Andel Research Institute, Grand Rapids, Michigan, United States of America; Van Andel Institute Graduate School, Grand Rapids, Michigan, United States of America.
Van Andel Institute · US

Funding

MK-STYX: A Requisite Gatekeeper to Mitochondrial Function and DeathR01CA138651 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI MACKEIGAN, JEFFREY PAUL · 2009 to 2013
$1.7M
NCI NIH HHS R01 CA138651NCI NIH HHS R01CA138651
6 · The paper itself

Abstract

Cancer cells have several hallmarks that define their neoplastic behavior. One is their unabated replicative potential that allows cells to continually proliferate, and thereby contribute to increasing tumor burden. The progression of a cell through the cell cycle is regulated by a series of checkpoints that ensures successful transmission of genetic information, as well as various cellular components, including organelles and protein complexes to the two resulting daughter cells. The mitochondrial reticulum undergoes coordinated changes in shape to correspond with specific stages of the cell cycle, the most dramatic being complete mitochondrial fragmentation prior to cytokinesis. To determine whether mitochondrial fission is a required step to ensure proper mitochondrial segregation into two daughter cells, we investigated the importance of mitochondrial dynamics to cell cycle progression. We found that mitochondrial hyperfusion promotes a defect in cell cycle progression characterized by an inability for cells to exit G2/M. Additionally, extended periods of persistent mitochondrial fusion led to robust caspase-dependent cell death. The cell death signals were coordinated through activation and cleavage of caspase-8, promoting a potent death response. These results demonstrate the importance of mitochondrial dynamics in cell cycle progression, and that inhibiting mitochondrial fission regulators may provide a therapeutic strategy to target the replicative potential of cancer cells.

Indexed as

ApoptosisCell DivisionG2 PhaseCaspasesCell Line, TumorCell SurvivalHumansMitochondriaCaspases

Identifiers

PMID24632851
PMCPMC3954829
OpenAlexW2031726907

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.