Evidence map›Paper›PMID 37466744›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2023

Targeting TRIM24 promotes neuroblastoma differentiation and decreases tumorigenicity via LSD1/CoREST complex.

Qiqi Shi, Bo Yu, Yingwen Zhang, Yi Yang, Chenxin Xu, Mingda Zhang, Guoyu Chen, Fei Luo, Bowen Sun, Ru Yang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
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

12 authors at 3 institutions in 1 country.

Qiqi ShiRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Bo YuRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Yingwen ZhangRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Yi YangPediatric Translational Medicine Institute, Department of Hematology & Oncology, Shanghai Children's Medical Center, School of Medicine, National Health Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai Jiao Tong University, Shanghai, 200127, China.
Chenxin XuRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Mingda ZhangRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Guoyu ChenRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Fei LuoRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Bowen SunRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Ru YangRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China.
Yanxin LiPediatric Translational Medicine Institute, Department of Hematology & Oncology, Shanghai Children's Medical Center, School of Medicine, National Health Committee Key Laboratory of Pediatric Hematology & Oncology, Shanghai Jiao Tong University, Shanghai, 200127, China. liyanxin@scmc.com.cn.
Haizhong FengRenji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University, Shanghai, 200127, China. fenghaizhong@sjtu.edu.cn.
Shanghai Cancer Institute · CNShanghai Jiao Tong University · CNShanghai Children's Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHigh-risk neuroblastoma (NB) still has an unfavorable prognosis and inducing NB differentiation is a potential strategy in clinical treatment, yet underlying mechanisms are still elusive. Here we identify TRIM24 as an important regulator of NB differentiation.

methodsMultiple datasets and clinical specimens were analyzed to define the role of TRIM24 in NB. The effects of TRIM24 on differentiation and growth of NB were determined by cell morphology, spheres formation, soft agar assay, and subcutaneous xenograft in nude mice. RNA-Seq and qRT-PCR were used to identify genes and pathways involved. Mass spectrometry and co-immunoprecipitation were used to explore the interaction of proteins.

resultsTrim24 is highly expressed in spontaneous NB in TH-MYCN transgenic mice and clinical NB specimens. It is associated with poor NB differentiation and unfavorable prognostic. Knockout of TRIM24 in neuroblastoma cells promotes cell differentiation, reduces cell stemness, and inhibits colony formation in soft agar and subcutaneous xenograft tumor growth in nude mice. Mechanistically, TRIM24 knockout alters genes and pathways related to neural differentiation and development by suppressing LSD1/CoREST complex formation. Besides, TRIM24 knockout activates the retinoic acid pathway. Targeting TRIM24 in combination with retinoic acid (RA) synergistically promotes NB cell differentiation and inhibits cell viability.

conclusionOur findings demonstrate that TRIM24 is critical for NB differentiation and suggest that TRIM24 is a promising therapeutic target in combination with RA in NB differentiation therapy.

Indexed as

NeuroblastomaAgarAnimalsCarrier ProteinsCell DifferentiationCell Line, TumorGene Expression Regulation, NeoplasticHistone DemethylasesHumansMiceMice, KnockoutMice, NudeMice, TransgenicTretinoinAgarCarrier ProteinsHistone DemethylasesTretinoinTRIM24 protein, humanDifferentiationLSD1NeuroblastomaRetinoic acidTRIM24

Identifiers

PMID37466744
PMCPMC12974650
OpenAlexW4384665352

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.