Evidence map›Paper›PMID 40973819›Full record

ArticleNature metabolism2025

Fructose and glucose from sugary drinks enhance colorectal cancer metastasis via SORD.

Tianshi Feng, Qin Luo, Yanlin Liu, Zeyu Jin, David Skwarchuk, Rumi Lee, Miso Nam, John M Asara, Daya R Adye, Philip L Lorenzi and 9 more

Abstract read
In one paragraph

Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

19 authors.

Tianshi Feng *Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Qin Luo *Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Yanlin LiuDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Zeyu JinDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
David SkwarchukDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Rumi LeeDepartment of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Miso NamDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0001-8202-9541
John M AsaraDivision of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0001-7450-2589
Daya R AdyeDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Philip L LorenziMetabolomics Core Facility, Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0003-0385-7774
Lin TanMetabolomics Core Facility, Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Guangsheng PeiCenter for Precision Health, McWilliams School of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Zhongming ZhaoCenter for Precision Health, McWilliams School of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, USA.ORCID http://orcid.org/0000-0002-3477-0914
Neda Zarrin-KhamehDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, TX, USA.
Adriana Paulucci-HolthauzenDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Brian W SimonsCenter for Comparative Medicine, Baylor College of Medicine, Houston, TX, USA.
Ju-Seog LeeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Scott KopetzDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jihye YunDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. jyun@mdanderson.org.ORCID http://orcid.org/0000-0001-5709-8254

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI JENNIFER W MACK · 1985 to 2026
$330.6M
Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
ROLE OF SORD IN SUGAR-MEDIATED CANCER METASTASISR01CA262437 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Jihye Yun · 2022 to 2026
$1.5M
Impact of sugary drinks on gut microbiota and development of young-onset colorectal cancerR21CA258134 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YUN, JIHYE · 2021 to 2021
$411k
NCI NIH HHS P01 CA120964NCI NIH HHS P30 CA006516NCI NIH HHS R01 CA262437NCI NIH HHS R21 CA258134Pew Charitable Trusts Pew-Stewart ScholarU.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA262437U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R21CA258134V Foundation for Cancer Research (V Foundation) V Sholar
6 · The paper itself

Abstract

The consumption of sugar-sweetened beverages (SSBs), which contain high levels of fructose and glucose, has been causally and mechanistically linked to an increased risk of colorectal cancer (CRC). However, the effects of SSB consumption on advanced stages of disease progression, including metastasis, remain poorly understood. Here we show that exposure of CRC cells to a glucose and fructose formulation-reflecting the composition of both high-fructose corn syrup and sucrose found in SSBs-enhances cellular motility and metastatic potential compared to glucose alone. Given that CRC cells grow poorly in fructose alone, and cells in vivo are not physiologically exposed to fructose without glucose, we excluded the fructose-only condition from our studies unless needed as a control. Mechanistically, the combination of glucose and fructose elevates the NAD⁺/NADH ratio by activation of the reverse reaction of sorbitol dehydrogenase in the polyol pathway. This redox shift relieves NAD⁺ limitations and accelerates glycolytic activity, which in turn fuels activation of the mevalonate pathway, ultimately promoting CRC cell motility and metastasis. Our findings highlight the detrimental impact of SSBs on CRC progression and suggest potential dietary and therapeutic strategies to mitigate metastasis in patients with CRC.

Indexed as

Colorectal NeoplasmsFructoseGlucoseSugar-Sweetened BeveragesAnimalsCell Line, TumorCell MovementGlycolysisHumansMiceNADNeoplasm MetastasisFructoseGlucoseNAD

Identifiers

PMID40973819
PMCPMC12552132

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.