Evidence map›Paper›PMID 41203613›Full record

ArticleCell death discovery2025

MDMX reprograms glycolysis of hepatocellular carcinoma via 14-3-3γ/FOXO1.

Han Chen, Qilong Pan, Meiqi Mao, Wu Lin, Sisi Yan, Jie Liu, Shuoqi Lin, Qin Li, Sihui Xue, Yixuan Xie and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 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

14 authors.

Han Chen *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Qilong Pan *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Meiqi Mao *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Wu LinDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Sisi YanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Jie LiuDepartment of Endoscopic Center, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China.ORCID http://orcid.org/0000-0003-3307-1975
Shuoqi LinFujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Qin LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Sihui XueDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Yixuan XieDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Lincan DingFujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Dali ZhengFujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China. DaliZheng@fjmu.edu.cn.ORCID http://orcid.org/0000-0003-2345-4040
Jie YouDepartment of Endocrinology and Metabolism, Fujian Medical University Union Hospital, Fuzhou, China. youjie@fjmu.edu.cn.
Qingling HuangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China. QinglingHuang@fjmu.edu.cn.ORCID http://orcid.org/0000-0002-0538-8249

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172911
6 · The paper itself

Abstract

MDMX serves as a significant regulator of p53, which is a crucial tumor suppressor protein. However, the biological functions and underlying mechanism of MDMX in hepatocellular carcinoma (HCC) remain inadequately understood. In this study, we demonstrate that MDMX is overexpressed in HCC, and elevated expression of MDMX is significantly correlated with poor prognosis in HCC harboring mutant p53. MDMX inhibits the degradation of 14-3-3γ and facilitates its localization within cytoplasm, thereby enhances the interaction between FOXO1 and 14-3-3γ, which promotes the degradation of FOXO1. Consequently, the overexpression of MDMX results in downregulation of FOXO1 followed by increase of RPIA and decrease of PCK1, leading to increased glucose uptake, lactate secretion, and ATP production. These findings elucidate the role of MDMX in promoting glycolysis through the regulation of the 14-3-3γ/FOXO1 axis in p53-mutated HCC, thereby offering a potential therapeutic target for the treatment of HCC.

Identifiers

PMID41203613
PMCPMC12595022

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