Evidence map›Paper›PMID 39722173›Full record

ArticleCancer communications (London, England)2025

Orchestrated desaturation reprogramming from stearoyl-CoA desaturase to fatty acid desaturase 2 in cancer epithelial-mesenchymal transition and metastasis.

Zhicong Chen, Yanqing Gong, Fukai Chen, Hyeon Jeong Lee, Jinqin Qian, Jing Zhao, Wenpeng Zhang, Yamin Li, Yihui Zhou, Qiaobing Xu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer communications (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 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

13 authors.

Zhicong ChenDepartment of Obstetrics and Gynecology, Center for Reproductive Medicine, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, P. R. China.ORCID 0000-0002-7549-4696
Yanqing GongDepartment of Urology, Peking University First Hospital, Beijing, P. R. China.
Fukai ChenDepartment of Biomedical Engineering, Department of Electrical and Computer Engineering, Photonics Center, Boston University, Boston, Massachusetts, USA.
Hyeon Jeong LeeDepartment of Biomedical Engineering, Department of Electrical and Computer Engineering, Photonics Center, Boston University, Boston, Massachusetts, USA.
Jinqin QianDepartment of Urology, Peking University First Hospital, Beijing, P. R. China.
Jing ZhaoMOE Key Laboratory of Bioorganic Phosphorus Chemistry & Chemical Biology, Department of Chemistry, Tsinghua University, Beijing, P. R. China.
Wenpeng ZhangState Key Laboratory of Precision Measurement Technology and Instruments, Department of Precision Instrument, Tsinghua University, Beijing, P. R. China.
Yamin LiDepartment of Biomedical Engineering, Tufts University, Medford, Massachusetts, USA.
Yihui ZhouCollege of Biomedical Engineering & Instrument Science, Key Laboratory for Biomedical Engineering of Ministry of Education, Zhejiang University, Hangzhou, Zhejiang, P. R. China.
Qiaobing XuDepartment of Biomedical Engineering, Tufts University, Medford, Massachusetts, USA.
Yu XiaMOE Key Laboratory of Bioorganic Phosphorus Chemistry & Chemical Biology, Department of Chemistry, Tsinghua University, Beijing, P. R. China.
Liqun ZhouDepartment of Urology, Peking University First Hospital, Beijing, P. R. China.
Ji-Xin ChengDepartment of Biomedical Engineering, Department of Electrical and Computer Engineering, Photonics Center, Boston University, Boston, Massachusetts, USA.

Funding

Advanced laser scanning confocal microscope for multiple usersS10OD024993 · OD · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI MERTZ, JEROME · 2018 to 2018
$448k
China Postdoctoral Science Foundation 2022M710895Guangdong Basic and Applied Basic Research Foundation 2024A1515013031National Natural Science Foundation of China 82173216National Natural Science Foundation of China 82203709National Natural Science Foundation of China 82372950National Natural Science Foundation of China 82372951NIH HHS S10 OD024993
6 · The paper itself

Abstract

backgroundAdaptative desaturation in fatty acid (FA) is an emerging hallmark of cancer metabolic plasticity. Desaturases such as stearoyl-CoA desaturase (SCD) and fatty acid desaturase 2 (FADS2) have been implicated in multiple cancers, and their dominant and compensatory effects have recently been highlighted. However, how tumors initiate and sustain their self-sufficient FA desaturation to maintain phenotypic transition remains elusive. This study aimed to explore the molecular orchestration of SCD and FADS2 and their specific reprogramming mechanisms in response to cancer progression.

methodsThe potential interactions between SCD and FADS2 were explored by bioinformatics analyses across multiple cancer cohorts, which guided subsequent functional and mechanistic investigations. The expression levels of desaturases were investigated with online datasets and validated in both cancer tissues and cell lines. Specific desaturation activities were characterized through various isomer-resolved lipidomics methods and sensitivity assays using desaturase inhibitors. In-situ lipid profiling was conducted using multiplex stimulated Raman scattering imaging. Functional assays were performed both in vitro and in vivo, with RNA-sequencing employed for the mechanism verification.

resultsAfter integration of the RNA-protein-metabolite levels, the data revealed that a reprogramming from SCD-dependent to FADS2-dependent desaturation was linked to cancer epithelial-mesenchymal transition (EMT) and progression in both patients and cell lines. FADS2 overexpression and SCD suppression concurrently maintained EMT plasticity. A FADS2/β-catenin self-reinforcing feedback loop facilitated the degree of lipid unsaturation, membrane fluidity, metastatic potential and EMT signaling. Moreover, SCD inhibition triggered a lethal apoptosis but boosted survival plasticity by inducing EMT and enhancing FA uptake via adenosine monophosphate-activated protein kinase activation. Notably, this desaturation reprogramming increased transforming growth factor-β2, effectively sustaining aggressive phenotypes and metabolic plasticity during EMT.

conclusionsThese findings revealed a metabolic reprogramming from SCD-dependent to FADS2-dependent desaturation during cancer EMT and progression, which concurrently supports EMT plasticity. Targeting desaturation reprogramming represents a potential vulnerability for cancer metabolic therapy.

Indexed as

Epithelial-Mesenchymal TransitionFatty Acid DesaturasesNeoplasmsStearoyl-CoA DesaturaseAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceNeoplasm MetastasisFADS2 protein, humanFatty Acid DesaturasesStearoyl-CoA Desaturasecancer metastasisepithelial‐mesenchymal transitionfatty acid desaturase 2metabolic reprogrammingstearoyl‐CoA desaturase

Identifiers

PMID39722173
PMCPMC11947613

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.