Evidence map›Paper›PMID 41118283›Full record

ReviewHepatology communications2025

Lipid metabolism in cancer cells: Its role in hepatocellular carcinoma progression and therapeutic resistance.

Tin Lok Wong, Yanshu Kong, Stephanie Ma

Abstract readReview
In one paragraph

Review in Hepatology communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Advances in Lipid Metabolism Reprogramming in Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Simvastatin Restores Cisplatin Sensitivity by Suppressing the Caveolin-1-Mediated PI3K/AKT Signaling Pathway in Cisplatin-Resistant Cervical Cancer Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. 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

3 authors.

Tin Lok WongSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0003-1147-7958
Yanshu KongSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Stephanie MaSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver cancer, with hepatocellular carcinoma (HCC) as its predominant form, remains among the deadliest malignancies worldwide. Despite the expanding array of treatment options, current therapies benefit only a limited subset of patients. Metabolic reprogramming is a hallmark of cancer, with lipid metabolism playing a pivotal role in tumor progression, metastasis, and therapy resistance. HCC is profoundly influenced by alterations in lipid metabolic pathways, notably those involved in steatotic liver disease, a major risk factor. Key aspects such as de novo lipogenesis, lipid uptake, fatty acid oxidation, lipid peroxidation, biosynthesis of bioactive lipids, and cholesterol biosynthesis are all reprogrammed in liver cancer cells. These metabolic shifts modify the cancer cell lipidome-altering fatty acid unsaturation levels and other lipid profiles-to promote survival and resistance during therapy. Recent technological advances have deepened our understanding of dysregulated lipid metabolism in HCC. In this review, we examine how various facets of lipid metabolism contribute to HCC disease progression and resistance to standard treatments, including tyrosine kinase inhibitors, immune checkpoint inhibitors, and radiotherapy. We also explore the potential of targeting lipid metabolic pathways to enhance therapeutic efficacy and overcome resistance, highlighting dietary interventions as a promising, low-cost, low-side-effect strategy to resensitize resistant HCC cells.

Indexed as

Carcinoma, HepatocellularDrug Resistance, NeoplasmLipid MetabolismLiver NeoplasmsDisease ProgressionHumansLipogenesischemotherapyhepatocellular carcinomaimmunotherapylipid metabolismradiotherapytargeted therapytherapeutic resistance

Identifiers

PMID41118283
PMCPMC12548999

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.