Evidence map›Paper›PMID 37904237›Full record

ArticleGenome biology2023

Landscape of enhancer disruption and functional screen in melanoma cells.

Zhao Wang, Menghan Luo, Qian Liang, Ke Zhao, Yuelin Hu, Wei Wang, Xiangling Feng, Bolang Hu, Jianjin Teng, Tianyi You and 15 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. ePerturbDB: enhancer's experimental perturbation database.Database : the journal of biological databases and curation · 2026
    Article
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  5. Article
  6. Article
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  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Harnessing the evolving CRISPR/Cas9 for precision oncology.Journal of translational medicine · 2024
    Review
  14. 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

25 authors at 4 institutions in 1 country.

Zhao Wang *Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China. wangzhao19880923@wmu.edu.cn.
Menghan Luo *Department of Epidemiology and Biostatistics, Tianjin Key Laboratory of Molecular Cancer Epidemiology, The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Qian Liang *Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Ke Zhao *Department of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yuelin HuOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Wei WangDepartment of Epidemiology and Biostatistics, Tianjin Key Laboratory of Molecular Cancer Epidemiology, The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Xiangling FengDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Bolang HuOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Jianjin TengDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Tianyi YouDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Ran LiOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Zhengkai BaoOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Wenhao PanOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Tielong YangDepartment of Bone and Soft Tissue Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Chao ZhangDepartment of Bone and Soft Tissue Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Ting LiDepartment of Bone and Soft Tissue Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Xiaobao DongDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Xianfu YiDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Ben LiuDepartment of Epidemiology and Biostatistics, Tianjin Key Laboratory of Molecular Cancer Epidemiology, The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Li ZhaoDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Miaoxin LiZhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Kexin ChenDepartment of Epidemiology and Biostatistics, Tianjin Key Laboratory of Molecular Cancer Epidemiology, The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Weihong SongOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, China. weihong@wmu.edu.cn.
Jilong YangDepartment of Bone and Soft Tissue Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China. yangjilong@tjmuch.com.
Mulin Jun LiDepartment of Epidemiology and Biostatistics, Tianjin Key Laboratory of Molecular Cancer Epidemiology, The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China. mulinli@connect.hku.hk.ORCID 0000-0003-3598-3679
Tianjin Medical University Cancer Institute and Hospital · CNWenzhou Medical University · CNTianjin Medical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe high mutation rate throughout the entire melanoma genome presents a major challenge in stratifying true driver events from the background mutations. Numerous recurrent non-coding alterations, such as those in enhancers, can shape tumor evolution, thereby emphasizing the importance in systematically deciphering enhancer disruptions in melanoma.

resultsHere, we leveraged 297 melanoma whole-genome sequencing samples to prioritize highly recurrent regions. By performing a genome-scale CRISPR interference (CRISPRi) screen on highly recurrent region-associated enhancers in melanoma cells, we identified 66 significant hits which could have tumor-suppressive roles. These functional enhancers show unique mutational patterns independent of classical significantly mutated genes in melanoma. Target gene analysis for the essential enhancers reveal many known and hidden mechanisms underlying melanoma growth. Utilizing extensive functional validation experiments, we demonstrate that a super enhancer element could modulate melanoma cell proliferation by targeting MEF2A, and another distal enhancer is able to sustain PTEN tumor-suppressive potential via long-range interactions.

conclusionsOur study establishes a catalogue of crucial enhancers and their target genes in melanoma growth and progression, and illuminates the identification of novel mechanisms of dysregulation for melanoma driver genes and new therapeutic targeting strategies.

Indexed as

Enhancer Elements, GeneticMelanomaHumansMutationEnhancerHighly recurrent regions (HRRs)MelanomaMyocyte enhancer factor 2A (MEF2A)Phosphatase and tensin homolog (PTEN)

Identifiers

PMID37904237
PMCPMC10614365
OpenAlexW4388033628

What Socratic 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 Socratic graph.