Evidence map›Paper›PMID 41439972›Full record

ArticleCells2025

Utility of Tumor Suppressor E2F Target Gene Promoter Elements to Drive Gene Expression Specifically in Cancer Cells.

Kenta Kurayoshi, Masakazu Tanaka, Rinka Nakajima, Yaxuan Zhou, Mashiro Shirasawa, Mariana Fikriyanti, Jun-Ichi Fujisawa, Ritsuko Iwanaga, Andrew P Bradford, Keigo Araki and 1 more

Abstract read
In one paragraph

Article in Cells, 2025. 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

11 authors.

Kenta KurayoshiDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.
Masakazu TanakaDivision of Neuroimmunology, Joint Research Center for Human Retrovirus Infection, Kagoshima University, Kagoshima 890-8544, Kagoshima, Japan.ORCID 0000-0003-4098-385X
Rinka NakajimaDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.ORCID 0009-0000-3222-7590
Yaxuan ZhouDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.ORCID 0009-0009-2593-3572
Mashiro ShirasawaDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.ORCID 0009-0000-5743-7842
Mariana FikriyantiDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.
Jun-Ichi FujisawaDepartment of Microbiology, Kansai Medical University, Hirakata 570-8506, Osaka, Japan.
Ritsuko IwanagaDepartment of Obstetrics and Gynecology, University of Colorado School of Medicine, Anschutz Medical Campus, 12700 East 19th Avenue, Aurora, CO 80045, USA.ORCID 0009-0008-1142-4753
Andrew P BradfordDepartment of Obstetrics and Gynecology, University of Colorado School of Medicine, Anschutz Medical Campus, 12700 East 19th Avenue, Aurora, CO 80045, USA.ORCID 0000-0002-8728-571X
Keigo ArakiDepartment of Morphological Biology, Ohu University School of Dentistry, 31-1 Misumido Tomitamachi, Koriyama 963-8611, Fukushima, Japan.
Kiyoshi OhtaniDepartment of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan.

Funding

the Ministry of Education, Culture, Sports, Science and Technology in Japan 21K07136
6 · The paper itself

Abstract

The transcription factor E2F is the principal target of the tumor suppressor pRB. In almost all cancers, pRB function is disabled due to oncogenic changes, leading to enhanced E2F activity, thereby facilitating aberrant cell proliferation. Enhanced E2F activity has been utilized to drive gene expression preferentially in cancer cells using E2F target promoters, such as the E2F1 promoter. However, these promoters are also activated by physiological E2F activity in normal proliferating cells, resulting in gene expression in normal proliferating cells. In contrast, promoters of tumor suppressor genes, such

Indexed as

E2F Transcription FactorsGene Expression Regulation, NeoplasticNeoplasmsPromoter Regions, GeneticAnimalsCell Line, TumorCell ProliferationE2F1 Transcription FactorHumansMiceMice, NudeTumor Protein p73E2F1 Transcription FactorE2F Transcription FactorsTumor Protein p73ARFcancer cell-specificderegulated E2Fnormal proliferating cellspRBTAp73

Identifiers

PMID41439972
PMCPMC12731185

What OpenQuestion holds

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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.