Evidence map›Paper›PMID 38012744›Full record

ArticleGenome biology2023

Cooperation of MLL1 and Jun in controlling H3K4me3 on enhancers in colorectal cancer.

Xiang Lin, Ji-Dong Chen, Chen-Yu Wang, Zhen Cai, Rui Zhan, Chen Yang, La-Ying Zhang, Lian-Yun Li, Yong Xiao, Ming-Kai Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Targeting the Epigenome in Colorectal Cancer.International journal of molecular sciences · 2026
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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

11 authors at 1 institution in 1 country.

Xiang Lin *Frontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Ji-Dong Chen *Frontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Chen-Yu Wang *Frontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Zhen CaiFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Rui ZhanFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Chen YangFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
La-Ying ZhangDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Lian-Yun LiFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
Yong XiaoDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China. xiaoyue0831@163.com.
Ming-Kai ChenDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China. kaimingchen@163.com.
Min WuFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, College of Life Sciences, Taikang Center for Life and Medical Sciences, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China. wumin@whu.edu.cn.ORCID 0000-0003-1372-4764
Wuhan University · CN

Funding

Hebei Provincial Key Research Projects 2020BCB007National Natural Science Foundation of China 3217050383National Natural Science Foundation of China 81972647
6 · The paper itself

Abstract

backgroundEnhancer dysregulation is one of the important features for cancer cells. Enhancers enriched with H3K4me3 have been implicated to play important roles in cancer. However, their detailed features and regulatory mechanisms have not been well characterized.

resultsHere, we profile the landscape of H3K4me3-enriched enhancers (m3Es) in 43 pairs of colorectal cancer (CRC) samples. M3Es are widely distributed in CRC and averagely possess around 10% of total active enhancers. We identify 1322 gain variant m3Es and 367 lost variant m3Es in CRC. The target genes of the gain m3Es are enriched in immune response pathways. We experimentally prove that repression of CBX8 and RPS6KA5 m3Es inhibits target gene expression in CRC. Furthermore, we find histone methyltransferase MLL1 is responsible for depositing H3K4me3 on the identified Vm3Es. We demonstrate that the transcription factor AP1/JUN interacts with MLL1 and regulates m3E activity. Application of a small chemical inhibitor for MLL1 activity, OICR-9429, represses target gene expression of the identified Vm3Es, enhances anti-tumor immunity and inhibits CRC growth in an animal model.

conclusionsTaken together, our study illustrates the genome-wide landscape and the regulatory mechanisms of m3Es in CRC, and reveals potential novel strategies for cancer treatment.

Indexed as

Colorectal NeoplasmsHistonesMyeloid-Lymphoid Leukemia ProteinProto-Oncogene Proteins c-junAnimalsEnhancer Elements, GeneticHistone-Lysine N-MethyltransferaseHumansTranscription Factor AP-1histone H3 trimethyl Lys4Histone-Lysine N-MethyltransferaseHistonesJUN protein, humanKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinProto-Oncogene Proteins c-junTranscription Factor AP-1Colorectal cancerEnhancersH3K4me3JUNMLL1

Identifiers

PMID38012744
PMCPMC10680327
OpenAlexW4389050252

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.