Evidence map›Paper›PMID 40586825›Full record

ReviewCellular oncology (Dordrecht, Netherlands)2025

Lipid metabolism in cancer stem cells: reprogramming, mechanisms, crosstalk, and therapeutic approaches.

Haksoo Lee, Sujin Park, Jongwon Lee, Chaeyoung Lee, Hyunkoo Kang, JiHoon Kang, Jung Sub Lee, Eunguk Shin, HyeSook Youn, BuHyun Youn

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular oncology (Dordrecht, Netherlands), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Review
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  4. Article
  5. Review
  6. Review
  7. Article
  8. Insights Into circRNA-Mediated Lipid Metabolism in Cancer Progression.Journal of cellular and molecular medicine · 2026
    Review
  9. Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
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  19. 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.

Haksoo Lee *Department of Biological Sciences, Pusan National University, Busan, 46241, Korea.
Sujin Park *Department of Integrated Biological Science, Pusan National University, Busan, 46241, Korea.
Jongwon LeeDepartment of Orthopaedic Surgery, Pusan National University Hospital, Busan, 46241, Korea.
Chaeyoung LeeDepartment of Chemistry, Pusan National University, Busan, 46241, Korea.
Hyunkoo KangDepartment of Neurosurgery, Yale School of Medicine, New Haven, CT, 06510, USA.
JiHoon KangDepartment of Physiology, College of Medicine, Yeungnam University, Daegu, 42415, Korea.
Jung Sub LeeDepartment of Orthopaedic Surgery, Pusan National University Hospital, Busan, 46241, Korea.
Eunguk ShinNuclear Science Research Institute, Pusan National University, Busan, 46241, Korea.
HyeSook YounDepartment of Integrative Bioscience and Biotechnology, Sejong University, Seoul, 05006, Korea. hsyoun@sejong.ac.kr.
BuHyun YounDepartment of Biological Sciences, Pusan National University, Busan, 46241, Korea. bhyoun72@pusan.ac.kr.

Funding

National Research Foundation of Korea NRF-2022R1A2C1009681National Research Foundation of Korea RS-2023-00207904
6 · The paper itself

Abstract

Cancer stem cells (CSCs) are a highly plastic subpopulation of tumor cells with capabilities for self-renewal, therapy resistance, and metastasis. Recent evidence highlights lipid metabolic reprogramming as a central mechanism supporting these malignant traits. This review synthesizes current findings on key lipid metabolic processes in CSCs-including lipid uptake via CD36, intracellular storage in lipid droplets, de novo fatty acid synthesis by fatty acid synthase (FASN), fatty acid oxidation (FAO) regulated by carnitine palmitoyltransferase 1A (CPT1A), and cholesterol biosynthesis through the mevalonate pathway. Although many of these pathways are active in bulk cancer cells, CSCs demonstrate greater functional reliance on them, leading to enhanced survival, redox balance, and adaptation to therapy. These metabolic preferences vary by cancer type, underscoring the need for context-specific approaches. Moreover, stromal components of the tumor microenvironment (TME), such as cancer-associated fibroblasts, adipocytes, and mesenchymal stem cells, modulate CSC lipid metabolism through paracrine signals and substrate transfer, reinforcing CSC maintenance and drug resistance. Therapeutic strategies targeting lipid metabolism-such as inhibition of SCD1, CPT1A, and HMG-CoA reductase-have shown promising preclinical results in selectively depleting CSC populations and sensitizing tumors to treatment. However, challenges remain in preserving normal stem cell function, which also depends on lipid pathways. This review underscores the emerging significance of lipid metabolism as both a hallmark and vulnerability of CSCs, offering opportunities for novel targeted cancer therapies.

Indexed as

Cellular ReprogrammingLipid MetabolismNeoplasmsNeoplastic Stem CellsAnimalsHumansTumor MicroenvironmentCancer stem cellsChemoresistanceLipid metabolismMetabolic reprogrammingTumor microenvironment

Identifiers

PMID40586825
PMCPMC12528255

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.