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February 26, 2026Cancer LettersOpen Access

YTHDF1-mediated RNA m1A methylation promotes malignant progression of hepatocellular carcinoma via regulating LRP5/Wnt-β-catenin axis

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Authors

XGXinyu GuHenan University of Science and TechnologyHZHua ZhouFirst Affiliated Hospital of Henan University of Science and TechnologyWCWenjuan ChenHenan University of Science and Technology

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Overview

The study demonstrates YTHDF1's regulation of LRP5 and Wnt-β-catenin, promoting HCC progression, suggesting a new therapeutic target.

Key Points

  • To investigate the role of YTHDF1-mediated RNA m1A methylation in hepatocellular carcinoma and its molecular mechanisms.
  • Integrated analysis of HCC data from The Cancer Genome Atlas (TCGA) and tissue microarray (TMA).
  • Functional experiments in vitro to assess proliferation and invasion of HCC cells upon YTHDF1 knockdown.
  • In vivo xenograft models to confirm findings from in vitro experiments.
  • MeRIP-seq and RNA-seq to analyze m1A modifications and their effects on mRNA stability.
  • Dual-luciferase reporter assays to evaluate YTHDF1's impact on LRP5 mRNA stability.
  • YTHDF1 expression is significantly higher in HCC tissues and correlates with poor patient prognosis.
  • Knockdown of YTHDF1 inhibits HCC cell proliferation and invasion both in vitro and in vivo.
  • LRP5 identified as a downstream target of YTHDF1 with confirmed binding to its mRNA.
  • YTHDF1 knockdown reduces levels of Wnt pathway components, inhibiting malignant traits in cells.
  • Overexpression of LRP5 reverses the effects caused by YTHDF1 knockdown.

Cite This Study

Gu et al. (2026) studied this question.

synapsesocial.com/papers/699fe36b95ddcd3a253e74fdhttps://doi.org/10.1016/j.canlet.2026.218353
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