ArticleExperimental hematology & oncology2021
YTHDF1 promotes hepatocellular carcinoma progression via activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition.
Article in Experimental hematology & oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed.
- YTHDF1 enhances ACSL3 translation in an m6A-dependent manner to regulate lipid metabolism and colorectal cancer progression.Translational cancer research · 2026Article
- YTHDF1/SLC39A4 signaling axis promotes gastric cancer cell proliferation by suppressing cuproptosis ex vivo and in vitro.Cancer gene therapy · 2026Article
- SULT1E1 suppresses hepatocellular carcinoma progression via activation of the TGF-β/SMAD signaling pathway and cell cycle arrest.BMC gastroenterology · 2026Article
- Anti-tumor Effects of Pollen Pini on Hepatocarcinoma SMMC-7721 Cells via Modulation of PI3K-Akt Signaling Pathway.Chinese journal of integrative medicine · 2026Article
- The Regulatory Role of mCells · 2026Review
- Epitranscriptomic control of epithelial-mesenchymal transition in cancer: mechanisms, plasticity, and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- New understanding of the molecular pathogenesis and therapeutic progress of hepatocellular carcinoma.Oncology reviews · 2026Review
- YTHDF1 regulates YTHDF2 stability via m6A-dependent mechanisms in hepatocellular carcinoma: insights fromJournal of gastrointestinal oncology · 2025Article
- Targeting m6A methylation for early diagnosis and precision medicine in hepatocellular carcinoma.Cancer cell international · 2025Review
- Identification of Androgen Receptor as a Molecular Docking Target for Survival and Response to Metformin-Induced Ferroptosis in Liver Cancer.Cancer reports (Hoboken, N.J.) · 2025Article
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
- MicroRNA Let-7b-5p Targets IGF1R to Inhibit the Progression of Hepatocellular Carcinoma Through the AKT/mTOR Pathway.Cancer medicine · 2025Article
- YTHDF1 shapes immune-mediated hepatitis via regulating inflammatory cell recruitment and response.Genes & diseases · 2025Article
- Effects of Benzo[a]Pyrene Exposure on Lung Cancer: A Mechanistic Study of Epigenetic m6A Levels and YTHDF1.Toxics · 2025Article
- Progress in the Application of Novel Nanomaterials in Targeted Therapy for Liver Cancer.International journal of nanomedicine · 2025Review
- Macrophage-derived exosome piR-50971 exacerbates sepsis-induced myocardial injury by inhibiting autophagy through the upregulation of N6-Methyladenosine modification of mTOR.Burns & trauma · 2025Article
- Mir-615-3p promotes osteosarcoma progression via the SESN2/AMPK/mTOR pathway.Cancer cell international · 2024Article
- YTHDF2 promotes anaplastic thyroid cancer progression by activating the DDIT4/AKT/mTOR signaling pathway.Biology direct · 2024Article
- N6-methyladenosine regulators in hepatocellular carcinoma: investigating the precise definition and clinical applications of biomarkers.Biology direct · 2024Article
- The YTH domain-containing protein family: Emerging players in immunomodulation and tumour immunotherapy targets.Clinical and translational medicine · 2024Review
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Authors and funding
4 authors.
Funding
Abstract
backgroundN
methodsBased on various bioinformatics databases, q-RT PCR, western blot, and a tissue microarray containing 90 HCC samples, we examined the expression of YTHDF1 in HCC. Then, we applied the loss-of-function experiments to explore the role of YTHDF1 in HCC by in vitro and in vivo assays. Finally, we performed the gene set enrichment analysis (GSEA) to predict the potential signaling pathway of YTHDF1 involved in HCC and further verified this prediction.
resultsYTHDF1 was overexpressed in HCC and associated with HCC grade. Depletion of YTHDF1 markedly impaired the proliferation, migration, invasion, and cell cycle process of HCC cells. Mechanistically, YTHDF1 promoted the growth of HCC cells via activating the PI3K/AKT/mTOR signaling pathway. Moreover, we also demonstrated that the epithelial-mesenchymal transition (EMT) mediated the promoting effect of YTHDF1 on the migration and invasion of HCC cells.
conclusionsYTHDF1 contributes to the progression of HCC by activating PI3K/AKT/mTOR signaling pathway and inducing EMT.
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