Evidence map›Paper›PMID 36362294›Full record

ArticleInternational journal of molecular sciences2022

Potential Therapeutic Effects of Thiazolidinedione on Malignant Glioma.

Meei-Ling Sheu, Liang-Yi Pan, Huai-Yun Hu, Hong-Lin Su, Jason Sheehan, Hsi-Kai Tsou, Hung-Chuan Pan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 8 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

7 authors at 4 institutions in 2 countries.

Meei-Ling SheuInstitute of Biomedical Sciences, National Chung-Hsing University, Taichung 402, Taiwan.ORCID 0000-0002-0431-1282
Liang-Yi PanFaculty of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Huai-Yun HuInstitute of Biomedical Sciences, National Chung-Hsing University, Taichung 402, Taiwan.
Hong-Lin SuDepartment of Life Sciences, Agriculture Biotechnology Center, National Chun-Hsing University, Taichung 402, Taiwan.
Jason SheehanDepartment of Neurosurgery, University of Virginia, Charlottesville, VA 22908, USA.
Hsi-Kai TsouDepartment of Neurosurgery, Taichung Veterans General Hospital, Taichung 40210, Taiwan.
Hung-Chuan PanInstitute of Biomedical Sciences, National Chung-Hsing University, Taichung 402, Taiwan.ORCID 0000-0003-3021-7676
National Chung Hsing University · TWKaohsiung Medical University · TWTaichung Veterans General Hospital · TWUniversity of Virginia · US

Funding

Taichung Veterans General Hospital TCVGH-1117303CTaichung Veterans General Hospital TCVGH-1117303DTaichung Veterans General Hospital TCVGH-PU1088103
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common and aggressive primary malignant tumor of the central nervous system. GBM has a very low 5-year survival rate and reaching merely a median of ~15 months even with aggressive treatments. PPARγ (Peroxisome proliferator- activated receptor gamma) agonists (ciglitazone), while being widely used on patients of type 2 diabetes mellitus, also have approved anticancer effects. Their action mechanisms on malignant glioma are not fully understood. The aim of this study is to investigate the potential therapeutic effect of PPARγ agonists on maligant glioma. Glioma cell line and in-vivo/ex-vivo animal model intervened by ciglitazone were used to assess the associated mechanism and therapeutic effect. Our results from in vivo and ex vivo experiments showed that ciglitazone not only inhibited tumor growth and its associated angiogenesis, but it also reduced colony formation and migration of tumors. Ciglitazone inhibited the phosphorylation of STAT3 (signal transducer and activator of transcription 3) (at the point of tyrosine 705 by increasing both the amount and activity of SHP-2 (Src homology region 2-containing protein tyrosine phosphatase 2) proteins, based on evidence obtained from immunoprecipitation and immunohistochemistry. Furthermore, ciglitazone activated proteasomes and lysosomes to degrade cell-cycle-related proteins like Cyclin D1, Cyclin E, CDK2 (Cyclin-dependent kinase 2), and CDK4 (Cyclin-dependent kinase 4). Ciglitazone triggered expressions of LC3 (Microtubule-associated protein 1A/1B-light chain 3) and formation of acidic vesicular organelles (AVOs), both of which were implicated in the autophagy pathway. In conclusion, ciglitazone showed the multiple actions to regulate the growth of glioma, which appeared to be a potential candidate for treating malignant glioma.

Indexed as

Diabetes Mellitus, Type 2GlioblastomaGliomaThiazolidinedionesAnimalsCell Cycle ProteinsCell Line, TumorHypoglycemic AgentsMicrotubule-Associated ProteinsPPAR gamma2,4-thiazolidinedioneCell Cycle ProteinsciglitazoneHypoglycemic AgentsMicrotubule-Associated ProteinsPPAR gammaThiazolidinedionesgliomaPPARγSHP-2STAT3thiazolidinedione

Identifiers

PMID36362294
PMCPMC9657575
OpenAlexW4308332186

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.