Evidence map›Paper›PMID 24027528›Full record

ReviewFrontiers in physiology2013

Intracellular ion channels and cancer.

Luigi Leanza, Lucia Biasutto, Antonella Managò, Erich Gulbins, Mario Zoratti, Ildikò Szabò

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 127 citations in OpenAlex.

  1. NaFrontiers in chemistry · 2026
    Article
  2. Article
  3. MCU-i4, a mitochondrial CaOncology research · 2025
    Article
  4. Article
  5. Chloride ions in health and disease.Bioscience reports · 2024
    Review
  6. Review
  7. Review
  8. Article
  9. Potassium Channels, Glucose Metabolism and Glycosylation in Cancer Cells.International journal of molecular sciences · 2023
    Review
  10. Frontiers in physiology · 2023
    Article
  11. T-type Ca2+ channels and their relationship with pre-neoplastic and neoplastic lesions in the human breast.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023
    Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022
    Review
  17. Article
  18. Review
  19. Article
  20. Discovery of KMedicinal research reviews · 2021
    Review

8 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

Luigi LeanzaDepartment of Biology, University of Padova Padova, Italy.
Lucia Biasutto
Antonella Managò
Erich Gulbins
Mario Zoratti
Ildikò Szabò
University of Padua · ITUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several types of channels play a role in the maintenance of ion homeostasis in subcellular organelles including endoplasmatic reticulum, nucleus, lysosome, endosome, and mitochondria. Here we give a brief overview of the contribution of various mitochondrial and other organellar channels to cancer cell proliferation or death. Much attention is focused on channels involved in intracellular calcium signaling and on ion fluxes in the ATP-producing organelle mitochondria. Mitochondrial K(+) channels (Ca(2+)-dependent BKCa and IKCa, ATP-dependent KATP, Kv1.3, two-pore TWIK-related Acid-Sensitive K(+) channel-3 (TASK-3)), Ca(2+) uniporter MCU, Mg(2+)-permeable Mrs2, anion channels (voltage-dependent chloride channel VDAC, intracellular chloride channel CLIC) and the Permeability Transition Pore (MPTP) contribute importantly to the regulation of function in this organelle. Since mitochondria play a central role in apoptosis, modulation of their ion channels by pharmacological means may lead to death of cancer cells. The nuclear potassium channel Kv10.1 and the nuclear chloride channel CLIC4 as well as the endoplasmatic reticulum (ER)-located inositol 1,4,5-trisphosphate (IP3) receptor, the ER-located Ca(2+) depletion sensor STIM1 (stromal interaction molecule 1), a component of the store-operated Ca(2+) channel and the ER-resident TRPM8 are also mentioned. Furthermore, pharmacological tools affecting organellar channels and modulating cancer cell survival are discussed. The channels described in this review are summarized on Figure 1. Overall, the view is emerging that intracellular ion channels may represent a promising target for cancer treatment.

Indexed as

apoptosiscancerion channelorganellespharmacology

Identifiers

PMID24027528
PMCPMC3759743
OpenAlexW1978314682

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.