Evidence map›Paper›PMID 42062634›Full record

ArticleFunctional & integrative genomics2026

Oncogenic DCTPP1/MYC feedback loop rewires pyrimidine metabolism to drive hepatocellular carcinoma.

Jing Li, Juan Liang, Meigui Zhang, Ruixia Ma, Ruili Zhou, Jiahui Xi, Haiying Yu, Yonghong Li, Chenyu Wang, Zhongtian Bai

Abstract read
PubMed Publisher
In one paragraph

Article in Functional & integrative genomics, 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. A Comprehensive Understanding ofCurrent issues in molecular biology · 2026
    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.

Jing Li *Key Laboratory of Biotherapy and Regenerative Medicine, The First School of Clinical Medicine, Lanzhou University, No. 1, Donggang West Road, Lanzhou, 730000, Gansu Province, China.
Juan Liang *Key Laboratory of Biotherapy and Regenerative Medicine, The First School of Clinical Medicine, Lanzhou University, No. 1, Donggang West Road, Lanzhou, 730000, Gansu Province, China.
Meigui Zhang *Gansu Provincial Hospital, Lanzhou, China.
Ruixia MaKey Laboratory of Biotherapy and Regenerative Medicine, The First School of Clinical Medicine, Lanzhou University, No. 1, Donggang West Road, Lanzhou, 730000, Gansu Province, China.
Ruili ZhouKey Laboratory of Biotherapy and Regenerative Medicine, The First School of Clinical Medicine, Lanzhou University, No. 1, Donggang West Road, Lanzhou, 730000, Gansu Province, China.
Jiahui XiKey Laboratory of Biotherapy and Regenerative Medicine, The First School of Clinical Medicine, Lanzhou University, No. 1, Donggang West Road, Lanzhou, 730000, Gansu Province, China.
Haiying YuKey Laboratory of Biotherapy and Regenerative Medicine, Lanzhou, Gansu Province, China.
Yonghong LiGansu Provincial Hospital, Lanzhou, China.
Chenyu WangInstitute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China.
Zhongtian BaiKey Laboratory of Biotherapy and Regenerative Medicine, The First School of Clinical Medicine, Lanzhou University, No. 1, Donggang West Road, Lanzhou, 730000, Gansu Province, China. ldyy_baizht@lzu.edu.cn.

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 82060666the Gansu Province Major Science and Technology Innovation Project in the Health Sector GSWSZD2024-01the Nature Science Foundation of Gansu Province (23JRRA1491
6 · The paper itself

Abstract

Nucleotide metabolic dysregulation fuels tumor proliferation, yet its drivers in hepatocellular carcinoma (HCC) remain poorly defined. DCTPP1, a dCTP pyrophosphohydrolase linked to aggressive cancers, is overexpressed in HCC but its regulatory role is unknown. Here, integrated analyses of clinical databases and tissue microarrays revealed that high DCTPP1 expression correlates with poor prognosis in HCC patients. Functional studies demonstrated that DCTPP1 knockdown suppresses HCC proliferation, migration, and tumorigenesis in vitro and in vivo. Mechanistically, we uncovered a novel DCTPP1-MYC positive feedback loop: MYC transcriptionally activates DCTPP1, while DCTPP1 modulates MYC protein levels, potentially through the Wnt/β-catenin signaling pathway. This circuit selectively disrupts pyrimidine metabolic enzymes (CTPS1, TYMS, TK1, NME1), destabilizing the dNTP pool and accelerating HCC progression. Our work identifies DCTPP1 as an oncogenic metabolic driver in HCC, revealing a targetable vulnerability for nucleotide metabolism-directed therapy.

Indexed as

Carcinoma, HepatocellularDeoxycytosine NucleotidesLiver NeoplasmsPyrophosphatasesAnimalsCell Line, TumorDNA ReplicationFeedbackGene Knockdown TechniquesHumansMiceMice, NudeProto-Oncogene Proteins c-mycPyrimidinesSignal TransductiondCTP pyrophosphataseDeoxycytosine NucleotidesMYC protein, humanProto-Oncogene Proteins c-mycPyrimidinesPyrophosphatasesDCTP pyrophosphohydrolase (DCTPP1)Hepatocellular carcinomaMYCOncogenePyrimidine metabolism

Identifiers

PMID42062634

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.