Evidence map›Paper›PMID 41054380›Full record

ArticleCancer science2025

Epigenetic Regulation of G6PD Drives Metabolic Reprogramming in Intrahepatic Cholangiocarcinoma.

Yusuke Nakano, Miwa Tanaka, Takeharu Sakamoto, Masahiro Hashimoto, Taro Tobo, Hideyuki Saito, Tadashi Abe, Tomohiko Ikehara, Takashi Ofuchi, Koto Kawata and 6 more

Abstract read
In one paragraph

Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

16 authors.

Yusuke NakanoDepartment of Surgery, Kyushu University Beppu Hospital, Oita, Japan.ORCID https://orcid.org/0009-0002-3588-2210
Miwa TanakaDepartment of Cancer Epigenomics, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID https://orcid.org/0000-0003-4934-3787
Takeharu SakamotoDepartment of Cancer Biology, Institute of Biomedical Science, Kansai Medical University, Osaka, Japan.ORCID https://orcid.org/0000-0002-1225-1902
Masahiro HashimotoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Taro ToboDepartment of Clinical Laboratory Medicine, Kyushu University Beppu Hospital, Oita, Japan.
Hideyuki SaitoDepartment of Surgery, Kyushu University Beppu Hospital, Oita, Japan.
Tadashi AbeDepartment of Surgery, Kyushu University Beppu Hospital, Oita, Japan.ORCID https://orcid.org/0000-0003-1153-6487
Tomohiko IkeharaDepartment of Surgery, Kyushu University Beppu Hospital, Oita, Japan.
Takashi OfuchiDepartment of Surgery, Kyushu University Beppu Hospital, Oita, Japan.
Koto KawataDepartment of Surgery, Kyushu University Beppu Hospital, Oita, Japan.
Takaaki MasudaDepartment of Breast and Endocrine Surgery, Kochi Medical School, Kochi University, Nankoku, Japan.ORCID https://orcid.org/0000-0002-6341-2438
Takayuki OginoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Mamoru UemuraDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Hidetoshi EguchiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.ORCID https://orcid.org/0000-0002-2318-1129
Yuichiro DokiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Koshi MimoriDepartment of Surgery, Kyushu University Beppu Hospital, Oita, Japan.ORCID https://orcid.org/0000-0003-3897-9974

Funding

Japan Agency for Medical Research and Development 22ama221501h0001Japan Agency for Medical Research and Development 23ck0106800h001OITA Cancer Research FoundationTakeda Science Foundation
6 · The paper itself

Abstract

Intrahepatic cholangiocarcinoma (ICC) is a highly aggressive malignancy with poor prognosis and significant molecular heterogeneity. This study investigates the role of tumor-specific enhancers in metabolic reprogramming, focusing on glucose-6-phosphate dehydrogenase (G6PD) and the pentose phosphate pathway (PPP). Using native elongating transcript-cap analysis of gene expression and single-cell RNA sequencing, tumor-specific enhancers driving G6PD overexpression were identified in ICC tumor epithelial cells. Functional assays demonstrated that G6PD promotes tumor proliferation by enhancing PPP activity and maintaining redox homeostasis, which provides NADPH to counter oxidative stress. Enhancer knockdown disrupted G6PD expression and PPP activity, increasing reactive oxygen species levels and reducing the NADPH/NADP

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaEpigenesis, GeneticGlucosephosphate DehydrogenaseAnimalsCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmEnhancer Elements, GeneticFemaleGene Expression Regulation, NeoplasticHumansMaleMetabolic ReprogrammingMiceCisplatinG6PD protein, humanGlucosephosphate DehydrogenaseNADPReactive Oxygen Speciescancer metabolismepigenetic regulationG6PDintrahepatic cholangiocarcinomapentose phosphate pathway

Identifiers

PMID41054380
PMCPMC12666459

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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.