ArticleProtein & cell2026
Lipid deposition promotes YTHDF3-mediated m6A modification of PPARα to facilitate liver metastasis of colorectal cancer.
Article in Protein & cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- Review
- The Molecular Signature of Early-Onset Colorectal Cancer Liver Metastases: Distinct Biology and Clinical Challenges.International journal of molecular sciences · 2026Review
- SREBP2-activated CNPY3 Phase Separation Promotes Colorectal Cancer by Enhancing MDM2-mediated p53 Degradation.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
The liver is a common site for cancer metastasis and a key metabolic organ. Lipid metabolism irregularities are linked to liver metastasis risk, but the mechanisms are not fully understood. Herein, in colorectal cancer liver metastasis (CRLM) clinical samples, lipid metabolism was broadly dysregulated, and lipid metabolites accumulated, as shown by integrated transcriptome and lipidomics analyses. Functionally, lipid deposition promotes liver metastasis in vitro and in vivo. Mechanistically, lipid deposition significantly enhances YTHDF3-mediated m6A modification and degradation of PPARα, which is crucial for liver metastasis. This process reduces the β-hydroxybutyrylation of YTHDF3, thereby promoting LLPS and increasing the stability of YTHDF3, which in turn facilitates the progression of CRC and liver metastasis. Furthermore, lipid deposition induces the interaction between STAT3 and YAP, activating YTHDF3 transcription. These two regulatory mechanisms synergize to drive YTHDF3 accumulation in lipid-rich metastatic lesions. In summary, our findings reveal that lipid deposition promotes LLPS-mediated m6A modification and decreases β-hydroxybutyrylation in liver metastasis, offering new strategies for the treatment of CRLM.
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Registered trials
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