Evidence map›Paper›PMID 38884661›Full record

ArticleJournal of neuro-oncology2024

TRIM37 interacts with EZH2 to epigenetically suppress PTCH1 and regulate stemness in glioma stem cells through sonic hedgehog pathway.

Lize Cai, Yongsheng Liu, Yanyan Li, Bin Liu, YuFei Cao, Wei Yang, Bo Wang, Ting Sun

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Article in Journal of neuro-oncology, 2024. 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
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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4 · The record

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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

8 authors.

Lize Cai *Neurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Yongsheng Liu *Neurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Yanyan LiNeurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Bin LiuDepartment of Neurosurgery, Qinghai Provincial People's Hospital, Xining, Qinghai, China.
YuFei CaoNeurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Wei YangState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection and Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, Jiangsu, China. detachedy@aliyun.com.
Bo Wang *Department of Oncology, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China. wangbo0622@126.com.
Ting SunNeurosurgery and Brain and Nerve Research Laboratory, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China. suntingst1979@126.com.

Funding

National Natural Science Foundation of China 32171234, 81874080, 31870844
6 · The paper itself

Abstract

backgroundGlioma stem cells (GSCs), which are known for their therapy resistance, play a substantial role in treatment inefficacy for glioblastoma multiforme (GBM). TRIM37, a member of the tripartite motif (TRIM) protein family initially linked to a rare growth disorder, has been recognized for its oncogenic role. However, the mechanism by which TRIM37 regulates tumor growth in glioma and GSCs is unclear.

methodsFor the in vitro experiments, gene expression was measured by western blotting, RT-qPCR, and immunofluorescence. Cell viability was detected by CCK-8, and cell apoptosis was detected by flow cytometry. The interaction between Enhancer of Zeste Homolog 2 (EZH2) and TRIM37 was verified by co-immunoprecipitation (Co-IP). The interaction between EZH2 and the PTCH1 promoter was verified using dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP). For the in vivo experiments, an orthotopically implanted glioma mouse model was used to validate tumor growth.

resultsThe expression of TRIM37 is higher in GSCs compared with matched non-GSCs. TRIM37 knockdown promotes apoptosis, decreased stemness in GSCs, and reduces tumor growth in GSCs xenografts of nude mice. TRIM37 and EZH2 co-localize in the nucleus and interact with each other. TRIM37 knockdown or EZH2 inhibition downregulates the protein expressions associated with the Sonic Hedgehog (SHH) pathway. EZH2 epigenetically downregulates PTCH1 to activate SHH pathway in GSCs.

conclusionsTRIM37 maintains the cell growth and stemness in GSCs through the interaction with EZH2. EZH2 activates SHH stem cell signaling pathway by downregulating the expression of SHH pathway suppressor PTCH1. Our findings suggest that TRIM37 may be a potential therapeutic target for GBM.

Indexed as

Brain NeoplasmsEnhancer of Zeste Homolog 2 ProteinGliomaHedgehog ProteinsNeoplastic Stem CellsPatched-1 ReceptorSignal TransductionTripartite Motif ProteinsUbiquitin-Protein LigasesAnimalsApoptosisCell Line, TumorCell ProliferationEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHedgehog ProteinsPatched-1 ReceptorPTCH1 protein, humanSHH protein, humanTRIM37 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesEZH2Glioma stem cellsPTCH1SHH pathwayTRIM37

Identifiers

PMID38884661

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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.