Evidence map›Paper›PMID 39406918›Full record

ArticleCell death and differentiation2024

AKR1B1-dependent fructose metabolism enhances malignancy of cancer cells.

Qing Zhao, Bing Han, Lu Wang, Jia Wu, Siliang Wang, Zhenxing Ren, Shouli Wang, Haining Yang, Michele Carbone, Changsheng Dong and 3 more

Abstract read
In one paragraph

Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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  4. Sex-Specific Regulation of Glycemic Homeostasis by Theabrownin from Pu-erh Tea.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

13 authors.

Qing Zhao *Center for Translational Medicine and Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
Bing Han *Mayo Clinic, 4500 San Pablo Rd S, Jacksonville, FL, 32224, USA.
Lu Wang *Department of Pharmacology and Pharmacy, University of Hong Kong, Hong Kong, China.ORCID 0000-0002-3918-3399
Jia WuCancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China.
Siliang WangCancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China.
Zhenxing RenCenter for Translational Medicine and Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
Shouli WangCenter for Translational Medicine and Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
Haining YangCancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI, 96813, USA.
Michele CarboneCancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI, 96813, USA.ORCID 0000-0001-8928-8474
Changsheng DongCancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China.
Gerry MelinoDepartment of Experimental Medicine, University of Rome "Tor Vergata", 00133, Rome, Italy. melino@uniroma2.it.ORCID 0000-0001-9428-5972
Wen-Lian ChenCancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. chenwl8412@shutcm.edu.cn.ORCID 0000-0002-1359-2549
Wei JiaCenter for Translational Medicine and Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China. weijia2@hku.hk.ORCID 0000-0002-3739-8994

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fructose metabolism has emerged as a significant contributor to cancer cell proliferation, yet the underlying mechanisms and sources of fructose for cancer cells remain incompletely understood. In this study, we demonstrate that cancer cells can convert glucose into fructose through a process called the AKR1B1-mediated polyol pathway. Inhibiting the endogenous production of fructose through AKR1B1 deletion dramatically suppressed glycolysis, resulting in reduced cancer cell migration, inhibited growth, and the induction of apoptosis and cell cycle arrest. Conversely, the acceleration of endogenous fructose through AKR1B1 overexpression has been shown to significantly enhance cancer cell proliferation and migration with increased S cell cycle progression. Our findings highlight the crucial role of endogenous fructose in cancer cell malignancy and support the need for further investigation into AKR1B1 as a potential cancer therapeutic target.

Indexed as

Cell ProliferationFructoseAldehyde ReductaseAldo-Keto ReductasesAnimalsApoptosisCell Line, TumorCell MovementGlucoseGlycolysisHumansMiceNeoplasmsAKR1B1 protein, humanAldehyde ReductaseAldo-Keto ReductasesFructoseGlucose

Identifiers

PMID39406918
PMCPMC11618507

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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.