Evidence map›Paper›PMID 33414520›Full record

ArticleCancer gene therapy2021

Inhibition of Gli2 suppresses tumorigenicity in glioblastoma stem cells derived from a de novo murine brain cancer model.

Seisuke Tanigawa, Mitsugu Fujita, Chiami Moyama, Shota Ando, Hiromi Ii, Yasushi Kojima, Teruaki Fujishita, Masahiro Aoki, Hayato Takeuchi, Takumi Yamanaka and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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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

13 authors at 4 institutions in 1 country.

Seisuke TanigawaDepartment of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.ORCID http://orcid.org/0000-0003-0107-5306
Mitsugu FujitaDepartment of Microbiology, Faculty of Medicine, Kindai University, Osaka, Japan.
Chiami MoyamaDepartment of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
Shota AndoDepartment of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
Hiromi IiDepartment of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
Yasushi KojimaDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Teruaki FujishitaDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Masahiro AokiDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.ORCID http://orcid.org/0000-0003-4316-9490
Hayato TakeuchiDepartment of Neurosurgery, Kyoto Prefectural University Graduate School of Medical Science, Kyoto, Japan.ORCID http://orcid.org/0000-0002-7260-6365
Takumi YamanakaDepartment of Neurosurgery, Kyoto Prefectural University Graduate School of Medical Science, Kyoto, Japan.
Yoshinobu TakahashiDepartment of Neurosurgery, Kyoto Prefectural University Graduate School of Medical Science, Kyoto, Japan.
Naoya HashimotoDepartment of Neurosurgery, Kyoto Prefectural University Graduate School of Medical Science, Kyoto, Japan.
Susumu NakataDepartment of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan. snakata@mb.kyoto-phu.ac.jp.ORCID http://orcid.org/0000-0002-9950-7543
Kyoto Prefectural University · JPKyoto Pharmaceutical University · JPAichi Cancer Center · JPKindai University · JP

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 16K08722MEXT | Japan Society for the Promotion of Science (JSPS) 20K07623
6 · The paper itself

Abstract

The prognosis of glioblastoma remains poor despite intensive research efforts. Glioblastoma stem cells (GSCs) contribute to tumorigenesis, invasive capacity, and therapy resistance. Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5), a stem cell marker, is involved in the maintenance of GSCs, although the properties of Lgr5-positive GSCs remain unclear. Here, the Sleeping-Beauty transposon-induced glioblastoma model was used in Lgr5-GFP knock-in mice identify GFP-positive cells in neurosphere cultures from mouse glioblastoma tissues. Global gene expression analysis showed that Gli2 was highly expressed in GFP-positive GSCs. Gli2 knockdown using lentiviral-mediated shRNA downregulated Hedgehog-related and Wnt signaling pathway-related genes, including Lgr5; suppressed tumor cell proliferation and invasion capacity; and induced apoptosis. Pharmacological Gli inhibition with GANT61 suppressed tumor cell proliferation. Silencing Gli2 suppressed the tumorigenicity of GSCs in an orthotopic transplantation model in vivo. These findings suggest that Gli2 affects the Hedgehog and Wnt pathways and plays an important role in GSC maintenance, suggesting Gli2 as a therapeutic target for glioblastoma treatment.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorCell ProliferationDisease Models, AnimalGene Expression ProfilingGlioblastomaHumansMicePrognosisZinc Finger Protein Gli2Gli2 protein, mouseZinc Finger Protein Gli2

Identifiers

PMID33414520
OpenAlexW3119839341

What OpenQuestion holds

Textmetadata
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.