Evidence map›Paper›PMID 37142416›Full record

ArticleCancer science2023

Therapeutic potential of pentamidine for glioma-initiating cells and glioma cells through multimodal antitumor effects.

Sho Tamai, Toshiya Ichinose, Shabierjiang Jiapaer, Nozomi Hirai, Hemragul Sabit, Shingo Tanaka, Masashi Kinoshita, Masahiko Kobayashi, Atsushi Hirao, Mitsutoshi Nakada

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. TetronicPharmaceutics · 2026
    Article
  4. Article
  5. Review
  6. 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.

Sho TamaiDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
Toshiya IchinoseDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
Shabierjiang JiapaerDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
Nozomi HiraiDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
Hemragul SabitDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
Shingo TanakaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
Masashi KinoshitaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
Masahiko KobayashiDivision of Molecular Genetics, Cancer Research Institute, Kanazawa University, Ishikawa, Japan.
Atsushi HiraoDivision of Molecular Genetics, Cancer Research Institute, Kanazawa University, Ishikawa, Japan.ORCID https://orcid.org/0000-0001-7818-8240
Mitsutoshi NakadaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.ORCID https://orcid.org/0000-0001-9419-6101
Kanazawa University · JP

Funding

Extramural Collaborative Research Grant of the Cancer Research Institute, Kanazawa UniversityIntramural Clinical Research Grant from Kanazawa University HospitalJapan Society for the Promotion of Science 20K17956Kobayashi International Scholarship Foundation
6 · The paper itself

Abstract

Glioma-initiating cells, which comprise a heterogeneous population of glioblastomas, contribute to resistance against aggressive chemoradiotherapy. Using drug reposition, we investigated a therapeutic drug for glioma-initiating cells. Drug screening was undertaken to select candidate agents that inhibit proliferation of two different glioma-initiating cells lines. The alteration of proliferation and stemness of the two glioma-initiating cell lines, and proliferation, migration, cell cycle, and survival of these two differentiated glioma-initiating cell lines and three different glioblastoma cell lines treated with the candidate agent were evaluated. We also used a xenograft glioma mouse model to evaluate anticancer effects of treated glioma cell lines. Among the 1301 agents, pentamidine-an antibiotic for Pneumocystis jirovecii-emerged as a successful antiglioma agent. Pentamidine treatment suppressed proliferation and stemness in glioma-initiating cell lines. Proliferation and migration were inhibited in all differentiated glioma-initiating cells and glioblastoma cell lines, with cell cycle arrest and caspase-dependent apoptosis induction. The in vivo study reproduced the same findings as the in vitro studies. Pentamidine showed a stronger antiproliferative effect on glioma-initiating cells than on differentiated cells. Western blot analysis revealed pentamidine inhibited phosphorylation of signal transducer and activator of transcription 3 in all cell lines, whereas Akt expression was suppressed in glioma-initiating cells but not in differentiated lines. In the present study, we identified pentamidine as a potential therapeutic drug for glioma. Pentamidine could be promising for the treatment of glioblastomas by targeting both glioma-initiating cells and differentiated cells through its multifaceted antiglioma effects.

Indexed as

Brain NeoplasmsGlioblastomaGliomaAnimalsApoptosisCell Line, TumorCell ProliferationHumansMicePentamidineXenograft Model Antitumor AssaysPentamidinedrug repositioninggliomaglioma-initiating cellpentamidineSTAT3

Identifiers

PMID37142416
PMCPMC10323113
OpenAlexW4368617751

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.