Evidence map›Paper›PMID 26161362›Full record

ReviewFrontiers in oncology2015

Mitochondrial Ca(2+) Remodeling is a Prime Factor in Oncogenic Behavior.

Alessandro Rimessi, Simone Patergnani, Massimo Bonora, Mariusz R Wieckowski, Paolo Pinton

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. MicroRNAs as Regulators of Cancer Cell Energy Metabolism.Journal of personalized medicine · 2022
    Review
  5. Review
  6. Review
  7. Alterations in the CaExploration of targeted anti-tumor therapy · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. 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

5 authors.

Alessandro RimessiSection of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), Department of Morphology, Surgery and Experimental Medicine, University of Ferrara , Ferrara , Italy.
Simone PatergnaniSection of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), Department of Morphology, Surgery and Experimental Medicine, University of Ferrara , Ferrara , Italy.
Massimo BonoraSection of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), Department of Morphology, Surgery and Experimental Medicine, University of Ferrara , Ferrara , Italy.
Mariusz R WieckowskiDepartment of Biochemistry, Nencki Institute of Experimental Biology , Warsaw , Poland.
Paolo PintonSection of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), Department of Morphology, Surgery and Experimental Medicine, University of Ferrara , Ferrara , Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is sustained by defects in the mechanisms underlying cell proliferation, mitochondrial metabolism, and cell death. Mitochondrial Ca(2+) ions are central to all these processes, serving as signaling molecules with specific spatial localization, magnitude, and temporal characteristics. Mutations in mtDNA, aberrant expression and/or regulation of Ca(2+)-handling/transport proteins and abnormal Ca(2+)-dependent relationships among the cytosol, endoplasmic reticulum, and mitochondria can cause the deregulation of mitochondrial Ca(2+)-dependent pathways that are related to these processes, thus determining oncogenic behavior. In this review, we propose that mitochondrial Ca(2+) remodeling plays a pivotal role in shaping the oncogenic signaling cascade, which is a required step for cancer formation and maintenance. We will describe recent studies that highlight the importance of mitochondria in inducing pivotal "cancer hallmarks" and discuss possible tools to manipulate mitochondrial Ca(2+) to modulate cancer survival.

Indexed as

Ca2+ signalingcancermitochondrial dysfunctiononcogene and oncosuppressor

Identifiers

PMID26161362
PMCPMC4479728

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.