Evidence map›Paper›PMID 40830415›Full record

ArticleNature cell biology2025

Systematic decoding of functional enhancer connectomes and risk variants in human glioma.

Jinfang Bi, Weipeng Mo, Man Liu, Yingjie Song, Qian Xiao, Sibo Fan, Wenbin Wang, Tengfei Shi, Yaoqiang Zheng, Jie Lian and 10 more

Abstract read
In one paragraph

Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Deciphering glioma susceptibility.Nature cell biology · 2025
    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

20 authors.

Jinfang Bi *Department of Laboratory Medicine and Institute of Precise Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Weipeng Mo *Department of Laboratory Medicine and Institute of Precise Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID http://orcid.org/0000-0002-2955-8310
Man Liu *State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Yingjie SongState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Qian XiaoDepartment of Laboratory Medicine and Institute of Precise Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Sibo FanState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Wenbin WangState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Tengfei ShiState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Yaoqiang ZhengState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Jie LianDepartment of Laboratory Medicine and Institute of Precise Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Rong LiuDepartment of Laboratory Medicine and Institute of Precise Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Bohan ChenState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Xiaofeng HuangState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Peng LiState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Zhongfang ZhaoState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Jiandang ShiState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Lei ZhangState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.ORCID http://orcid.org/0000-0003-4381-3696
Guangsong SuDepartment of Laboratory Medicine and Institute of Precise Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. sugs@mail.sysu.edu.cn.ORCID http://orcid.org/0009-0007-9819-3099
Nu ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. zhangnu2@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-2817-7065
Wange LuDepartment of Laboratory Medicine and Institute of Precise Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. lvwg@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-5848-3189

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32130018
6 · The paper itself

Abstract

Genetic and epigenetic variations contribute to the progression of glioma, but the mechanisms underlying these effects, particularly for enhancer-associated genetic variations in non-coding regions, still remain unclear. Here we performed high-throughput CRISPR interference screening to identify pro-tumour enhancers in glioma cells. By integrating genome-wide H3K27ac HiChIP data, we identified the target genes of these pro-tumour enhancers and revealed the essential role of enhancer connectomes in promoting glioma progression. Through systematic analysis of enhancers carrying glioma risk-associated single-nucleotide polymorphisms (SNPs), we found that these SNPs can promote glioma progression through the enhancer connectome. Using CRISPR-Cas9-mediated enhancer interference and SNP editing, we demonstrated that glioma-specific enhancer carrying the risk SNP rs2297440 regulates SOX18 expression by specifically recruiting transcription factor MEIS1 binding, thereby contributing to glioma progression. Our study sheds light on the molecular mechanisms underlying glioma susceptibility and provides potential therapeutic targets to treat glioma.

Indexed as

Brain NeoplasmsConnectomeEnhancer Elements, GeneticGliomaPolymorphism, Single NucleotideCell Line, TumorCRISPR-Cas SystemsDisease ProgressionGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansMyeloid Ecotropic Viral Integration Site 1 ProteinRisk FactorsMEIS1 protein, humanMyeloid Ecotropic Viral Integration Site 1 Protein

Identifiers

PMID40830415
PMCPMC12527947

What OpenQuestion holds

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Registered trials

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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.