Evidence map›Paper›PMID 40258813›Full record

ArticleCell death & disease2025

Targeted demethylation of the EphA7 promoter inhibits tumorigenesis via the SP1/DNMT1 and PI3K/AKT axes and improves the response to multiple therapies in cervical cancer.

Wenfan Zhang, Jing Zhao, Xueting Fan, Shuang Chen, Rong Wang

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Advances and clinical potential of epigenome editing.Cellular and molecular life sciences : CMLS · 2026
    Review
  2. Review
  3. Article
  4. DNMT Enzymes and Their Impact on Cervical Cancer: A State-of-the-Art Review.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. 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

5 authors.

Wenfan Zhang *Department of Laboratory Medicine, School of Medical Technology, Tianjin Medical University, Tianjin, China.
Jing Zhao *Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin, China.
Xueting FanDepartment of Laboratory Medicine, School of Medical Technology, Tianjin Medical University, Tianjin, China.
Shuang ChenDepartment of Laboratory Medicine, School of Medical Technology, Tianjin Medical University, Tianjin, China.
Rong WangDepartment of Laboratory Medicine, School of Medical Technology, Tianjin Medical University, Tianjin, China. wangrong825@tmu.edu.cn.ORCID http://orcid.org/0000-0003-3502-5446

Funding

Natural Science Foundation of Tianjin City (Natural Science Foundation of Tianjin) 23JCYBJC00230
6 · The paper itself

Abstract

Aberrant methylation of the EphA7 promoter has been observed in cervical cancer (CC); however, its precise function and role in CC remain largely unknown. In this study, we investigated the role and molecular mechanisms of EphA7 promoter methylation in cervical carcinogenesis. First, our results indicated that the reactivation of EphA7 expression via a CRISPR demethylation tool (dCas9-Tet1) had antitumor effects. It restrained tumor proliferation and invasion while promoting apoptosis via the PI3K/AKT signaling pathway in both CaSki and SiHa cells. The upstream interacting factors were subsequently captured by CRISPR-mediated pull-down in situ, and the result revealed that SP1 and MAZ interacted with the promoter of EphA7. However, the perturbation results revealed that EphA7 expression was associated with SP1/DNMT1 but not MAZ. Furthermore, 17-β-estradiol (E2) can upregulate EphA7 expression through demethylation via the SP1/DNMT1 axis. A rescue experiment revealed that interference with SP1 expression could restore the effect of E2 on increasing the expression of EphA7 by upregulating estrogen receptor expression. In addition, EphA7 demethylation reduced the half-maximal inhibitory concentration (IC

Indexed as

CarcinogenesisDNA (Cytosine-5-)-Methyltransferase 1Phosphatidylinositol 3-KinasesPromoter Regions, GeneticProto-Oncogene Proteins c-aktReceptor, EphA7Sp1 Transcription FactorUterine Cervical NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationDNA MethylationFemaleGene Expression Regulation, NeoplasticHumansDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, EphA7SP1 protein, humanSp1 Transcription Factor

Identifiers

PMID40258813
PMCPMC12012199

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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.