Evidence map›Paper›PMID 28410232›Full record

ArticleOncotarget2017

Vacquinol-1 inducible cell death in glioblastoma multiforme is counter regulated by TRPM7 activity induced by exogenous ATP.

Philip Sander, Haouraa Mostafa, Ayman Soboh, Julian M Schneider, Andrej Pala, Ann-Kathrin Baron, Barbara Moepps, C Rainer Wirtz, Michael Georgieff, Marion Schneider

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Roles of TRPM channels in glioma.Cancer biology & therapy · 2024
    Review
  3. Review
  4. Review
  5. The Role of TRPM7 in Oncogenesis.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Combined mTORC1/mTORC2 inhibition blocks growth and induces catastrophic macropinocytosis in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Transient Receptor Potential Cation Channels in Cancer Therapy.Medical sciences (Basel, Switzerland) · 2019
    Review
  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

10 authors at 1 institution in 1 country.

Philip SanderDivision of Experimental Anesthesiology, University Hospital Ulm, 89081 Ulm, Germany.
Haouraa MostafaDivision of Experimental Anesthesiology, University Hospital Ulm, 89081 Ulm, Germany.
Ayman SobohDivision of Experimental Anesthesiology, University Hospital Ulm, 89081 Ulm, Germany.
Julian M SchneiderDivision of Experimental Anesthesiology, University Hospital Ulm, 89081 Ulm, Germany.
Andrej PalaDepartment of Neurosurgery, Bezirkskrankenhaus Guenzburg, 89312 Guenzburg, Germany.
Ann-Kathrin BaronDepartment of Operative Dentistry and Periodontology, University Hospital Ulm, 89081 Ulm, Germany.
Barbara MoeppsInstitute of Pharmacology and Toxicology, University Hospital Ulm, 89081 Ulm, Germany.
C Rainer WirtzDepartment of Neurosurgery, Bezirkskrankenhaus Guenzburg, 89312 Guenzburg, Germany.
Michael GeorgieffDepartment of Anesthesiology, University Hospital Ulm, 89081 Ulm, Germany.
Marion SchneiderDivision of Experimental Anesthesiology, University Hospital Ulm, 89081 Ulm, Germany.
University Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastomas (GBM) are the most malignant brain tumors in humans and have a very poor prognosis. New therapeutic options are urgently needed. A novel drug, Vacquinol-1 (Vac), a quinolone derivative, displays promising properties by inducing rapid cell death in GBM but not in non-transformed tissues. Features of this type of cell death are compatible with a process termed methuosis. Here we tested Vac on a highly malignant glioma cell line observed by long-term video microscopy. Human dental-pulp stem cells (DPSCs) served as controls. A major finding was that an exogenous ATP concentration of as little as 1 μM counter regulated the Vac-induced cell death. Studies using carvacrol, an inhibitor of transient receptor potential cation channel, subfamily M, member 7 (TRPM7), demonstrated that the ATP-inducible inhibitory effect is likely to be via TRPM7. Exogenous ATP is of relevance in GBM with large necrotic areas. Our results support the use of GBM cultures with different grades of malignancy to address their sensitivity to methuosis. The video-microscopy approach presented here allows decoding of signaling pathways as well as mechanisms of chemotherapeutic resistance by long-term observation. Before implementing Vac as a novel therapeutic drug in GBM, cells from each individual patient need to be assessed for their ATP sensitivity. In summary, the current investigation supports the concept of methuosis, described as non-apoptotic cell death and a promising approach for GBM treatment. Tissue-resident ATP/necrosis may interfere with this cell-death pathway but can be overcome by a natural compound, carvacrol that even penetrates the blood-brain barrier.

Indexed as

Adenosine TriphosphateBrain NeoplasmsCaspase 3Caspase 7Cell DeathCell Line, TumorCymenesGene Expression Regulation, NeoplasticGlioblastomaHumansMonoterpenesPiperidinesProtein Serine-Threonine KinasesQuinolinesTRPM Cation ChannelsAdenosine TriphosphatecarvacrolCASP3 protein, humanCASP7 protein, humanCaspase 3Caspase 7CymenesMonoterpenesPiperidinesProtein Serine-Threonine KinasesQuinolinesTRPM7 protein, humanTRPM Cation Channelsvacquinol-1ATPglioblastoma multiformemethuosisTRPM7Vacquinol-1

Identifiers

PMID28410232
PMCPMC5471040
OpenAlexW2602492249

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.