ArticleInternational journal of genomics2025
P3H4 Enhances the Proliferation, Invasion, and Glycolysis of Hepatocellular Carcinoma Cells.
Article in International journal of genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Glycolytic reprogramming in endometriosis: molecular mechanisms, immune modulation, and non-hormonal therapeutic opportunities.BMC women's health · 2026Review
- γ-terpinene inhibits the progression of hepatocellular carcinoma by regulating the PTEN/PI3K/Akt signaling pathway mediated glycolysis.Scientific reports · 2026Article
- P3H4 Enhances the Proliferation, Invasion, and Glycolysis of Hepatocellular Carcinoma Cells.International journal of genomics · 2025Article
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8 authors.
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Abstract
Objective: The study is aimed at investigating the functions of P3H4 in liver cancer. Materials and Methods: The TCGA and CPTAC liver cancer databases were utilized to analyze the expression levels of P3H4 and its associated survival rates between tumor and normal tissues. A cohort of 60 HCC patients was selected based on criteria for P3H4 expression and survival analysis. qRT-PCR and western blotting techniques were employed to assess P3H4 expression in cell lines. The CCK8 assay was conducted to compare cell viability between normal and P3H4-knockdown HCC cell lines. A glycolysis detection kit was used to measure glucose, lactate, and ATP levels following P3H4 knockdown. A nude mouse tumorigenicity assay was performed by injecting Huh7 cells treated with sh-NC or sh-P3H4; tumor volume and weight were recorded, and tumor tissues were collected for IHC analysis. Results: P3H4 expression was found to be elevated in liver tumors compared to normal tissues, as indicated by both database analyses and patient data. High expression of P3H4 correlated with poorer survival and prognosis in patients. Knocking down P3H4 significantly inhibited HCC proliferation, invasion, glycolysis, and PI3K/AKT phosphorylation in HCC cell lines. Results from the nude mouse tumorigenicity assay demonstrated that the average tumor volume, tumor weight, and the percentage of Ki-67 positive cells were significantly reduced in the sh-P3H4 group compared to the sh-NC group. Conclusion: P3H4 promotes HCC proliferation, invasion, and glycolysis through the PI3K/AKT pathway, providing new insights into the diagnosis and treatment of HCC.
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