Evidence map›Paper›PMID 33824309›Full record

ArticleCell death & disease2021

MLL3 suppresses tumorigenesis through regulating TNS3 enhancer activity.

Jun-Yi Zheng, Chen-Yu Wang, Chuan Gao, Qiong Xiao, Cheng-Wei Huang, Min Wu, Lian-Yun Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. ELF5-Mediated Enhancer-Promoter Interaction Regulates LALBA Expression in Ovine Mammary Gland.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
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  5. Article
  6. Review
  7. Article
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  9. Article
  10. The molecular and clinical role of Tensin 1/2/3 in cancer.Journal of cellular and molecular medicine · 2023
    Review
  11. Review
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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

7 authors at 1 institution in 1 country.

Jun-Yi ZhengFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China.
Chen-Yu WangFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China.
Chuan GaoFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China.
Qiong XiaoFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China.
Cheng-Wei HuangFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China.
Min WuFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China. wumin@whu.edu.cn.ORCID 0000-0003-1372-4764
Lian-Yun LiFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China. lilianyun@whu.edu.cn.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MLL3 is a histone H3K4 methyltransferase that is frequently mutated in cancer, but the underlying molecular mechanisms remain elusive. Here, we found that MLL3 depletion by CRISPR/sgRNA significantly enhanced cell migration, but did not elevate the proliferation rate of cancer cells. Through RNA-Seq and ChIP-Seq approaches, we identified TNS3 as the potential target gene for MLL3. MLL3 depletion caused downregulation of H3K4me1 and H3K27ac on an enhancer ~ 7 kb ahead of TNS3. 3C assay indicated the identified enhancer interacts with TNS3 promoter and repression of enhancer activity by dCas9-KRAB system impaired TNS3 expression. Exogenous expression of TNS3 in MLL3 deficient cells completely blocked the enhanced cell migration phenotype. Taken together, our study revealed a novel mechanism for MLL3 in suppressing cancer, which may provide novel targets for diagnosis or drug development.

Indexed as

CarcinogenesisCell Transformation, NeoplasticDNA-Binding ProteinsEnhancer Elements, GeneticGene Expression Regulation, NeoplasticHistonesHumansPromoter Regions, GeneticTensinsDNA-Binding ProteinsHistonesKMT2C protein, humanTensinsTNS3 protein, human

Identifiers

PMID33824309
PMCPMC8024252
OpenAlexW3152487196

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.