Evidence map›Paper›PMID 41125417›Full record

ArticleCancer science2026

ZNF282 Promotes Colorectal Cancer Progression Possibly via E2F1 Activation.

Tadashi Abe, Takaaki Masuda, Taro Tobo, Masahiro Hashimoto, Yusuke Nakano, Hideyuki Saito, Takashi Ofuchi, Tomohiko Ikehara, Akinori Tsujimoto, Takafumi Nakano and 14 more

Abstract read
In one paragraph

Article in Cancer science, 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. 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

24 authors.

Tadashi AbeDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID https://orcid.org/0000-0003-1153-6487
Takaaki MasudaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID https://orcid.org/0000-0002-6341-2438
Taro ToboDepartment of Clinical Laboratory Medicine and Pathology, Kyushu University Beppu Hospital, Beppu, Japan.
Masahiro HashimotoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Yusuke NakanoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID https://orcid.org/0009-0002-3588-2210
Hideyuki SaitoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Takashi OfuchiDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Tomohiko IkeharaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Akinori TsujimotoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Takafumi NakanoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Katsushi DairakuDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Junichi TakahashiDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Kensuke KoikeDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID https://orcid.org/0000-0003-4428-2348
Koto KawataDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Yuki AndoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Kiyotaka HosodaDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Takanari TatsumiDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Kosuke HiroseDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Satoshi HiguchiDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Hajime OtsuDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Yusuke YonemuraDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.
Ken EtoDepartment of Surgery, The Jikei University School of Medicine, Tokyo, Japan.
Toru IkegamiDepartment of Surgery, The Jikei University School of Medicine, Tokyo, Japan.
Koshi MimoriDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Japan.ORCID https://orcid.org/0000-0003-3897-9974

Funding

Japan Agency for Medical Research and Development JP20cm0106475h0001Japan Society for the Promotion of Science 18K08649Japan Society for the Promotion of Science 19H03715Japan Society for the Promotion of Science JP19K09176Japan Society for the Promotion of Science JP20H05039Japan Society for the Promotion of Science JP20K08930Japan Society for the Promotion of Science JP20K17556Japan Society for the Promotion of Science JP22K08826Japan Society for the Promotion of Science JP22K08894Japan Society for the Promotion of Science JP22K09006Japan Society for the Promotion of Science JP23K07774Japan Society for the Promotion of Science JP23K08074Japan Society for the Promotion of Science JP23K08215Japan Society for the Promotion of Science JP24K10384Japan Society for the Promotion of Science JP24K11766Japan Surgical SocietyOITA Cancer Research FoundationPrincess Takamatsu Cancer Research FundTakeda Science FoundationUniversity of Tokyo
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, highlighting the urgent need for improved therapeutic strategies. In this study, we identified zinc finger protein 282 (ZNF282), located on chromosome 7q, as a novel gene that contributes to CRC progression through comprehensive expression profiling using data from The Cancer Genome Atlas (TCGA) and single-cell RNA sequencing combined with spatial transcriptomics in clinical CRC datasets. ZNF282 was overexpressed in tumor cells. High ZNF282 mRNA expression was associated with distant metastasis and served as an independent poor prognostic factor in CRC. In vitro and in vivo experiments using CRISPR/Cas9-mediated ZNF282 knockout CRC cell lines demonstrated significantly reduced tumor growth and cell proliferation, which were reversed by reexpression of ZNF282. Mechanistically, ZNF282 knockout impaired the G1/S cell cycle transition and downregulated E2F1 and its downstream targets, CCNE1 and CCND1. These findings were supported by single-cell RNA sequencing analysis, which showed ZNF282 enrichment in malignant epithelial cells linked to cell cycle pathways. Motif scanning further identified a putative ZNF282 binding site upstream of the E2F1 transcription start site, suggesting that ZNF282 may enhance E2F1 expression by facilitating the activity of an upstream regulatory region. In conclusion, ZNF282 is a novel gene that promotes CRC progression in part by enhancing cell cycle progression possibly via E2F1 activation. Its high expression is associated with poor prognosis, supporting its potential as a prognostic biomarker and therapeutic target in CRC.

Indexed as

Colorectal NeoplasmsE2F1 Transcription FactorAnimalsCell Line, TumorCell ProliferationCyclin D1Cyclin EDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceOncogene ProteinsPrognosisCCND1 protein, humanCCNE1 protein, humanCyclin D1Cyclin EE2F1 protein, humanE2F1 Transcription FactorOncogene Proteinscell cyclecell proliferationcolorectal cancerE2F1zinc finger protein 282 (ZNF282)

Identifiers

PMID41125417
PMCPMC12775571

What OpenQuestion holds

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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.