Evidence map›Paper›PMID 41461624›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2026

E2F8 Transcriptionally Activates DTL to Promote Endometrial Cancer Progression Via the MAPK Pathway.

Wenkang Tao, Jiaqi Pan, Wenqin Zhang, Yueyue Huang, Fenglin Bi, Xuemei Ding, Yuyun Jiang, Yuqian Ma, Yi Yang, Jifang Shi

Abstract read
PubMed Publisher
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Wenkang TaoDepartment of Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), Dali, Yunnan, 671000, P.R. China.
Jiaqi PanDepartment of Obstetrics and Gynecology, Huizhou Central People's Hospital, Huizhou, Guangdong, 516000, P.R. China.
Wenqin ZhangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), No. 32, Carlsberg Avenue, Dali, Yunnan, 671000, P.R. China.
Yueyue HuangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), No. 32, Carlsberg Avenue, Dali, Yunnan, 671000, P.R. China.
Fenglin BiDepartment of Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), Dali, Yunnan, 671000, P.R. China.
Xuemei DingDepartment of Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), Dali, Yunnan, 671000, P.R. China.
Yuyun JiangDepartment of Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), Dali, Yunnan, 671000, P.R. China.
Yuqian MaDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), No. 32, Carlsberg Avenue, Dali, Yunnan, 671000, P.R. China.
Yi YangDepartment of Clinical Medicine, Dali University, Dali, Yunnan, 671000, P.R. China.
Jifang ShiDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Dali University (Yunnan Provincial Fourth People's Hospital, Yunnan Provincial Second Infectious Disease Hospital), No. 32, Carlsberg Avenue, Dali, Yunnan, 671000, P.R. China. Sjffck@sina.com.ORCID 0009-0002-6772-6351

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E2F family transcription factors are involved in various cancers, yet the role of E2F transcription factor 8 (E2F8) in endometrial cancer (EC) remains elusive. This study explores how E2F8 transcriptionally activates denticleless E3 ubiquitin protein ligase homolog (DTL) to promote EC progression via the MAPK signaling. Bioinformatic analysis of the GEO dataset GSE63678, along with GEPIA2, AnimalTFDB v4, and ChIP-Atlas, identified E2F8 and its potential target DTL in EC. Elevated expression of E2F8 and DTL was confirmed in EC tissues, which correlated with a higher International Federation of Gynecology and Obstetrics stage. Functional assays demonstrated that E2F8 knockdown suppressed EC cell proliferation, migration, invasion, and MAPK pathway activation, while DTL overexpression or PDCD4 knockdown reversed these effects. Knockdown of DTL enhanced PDCD4 ubiquitination. In vivo, silencing of E2F8 inhibited tumor growth in EC xenograft models, whereas DTL upregulation or PDCD4 knockdown restored tumor progression and enhanced MAPK pathway activity and Ki67 expression. In conclusion, E2F8 promotes EC progression by transcriptionally activating DTL and activating the MAPK pathway. These findings provide novel mechanistic insights into EC progression and suggest that the E2F8/DTL/PDCD4/MAPK axis may serve as a potential therapeutic target for EC.

Indexed as

Endometrial NeoplasmsMAP Kinase Signaling SystemRepressor ProteinsUbiquitin-Protein LigasesAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeE2F8 protein, humanRepressor ProteinsUbiquitin-Protein LigasesDTLE2F8ECMAPK pathwayPDCD4 ubiquitination

Identifiers

PMID41461624

What OpenQuestion holds

Textmetadata
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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.