GTPBP4 is a GTP-binding protein with dual roles in ribosome biogenesis and cell cycle regulation. In the nucleolus, it participates in 60S ribosomal subunit assembly and acts as a negative regulator of innate immune responses by suppressing interferon-β production during viral infection 1. At the molecular level, GTPBP4 functions as a TP53 repressor, preventing p53 stabilization and cell cycle arrest. In cancer contexts, particularly hepatocellular carcinoma and colorectal carcinoma, GTPBP4 promotes tumor progression and metastasis through multiple mechanisms: it enhances aerobic glycolysis via PKM2 sumoylation 2, disrupts actin cytoskeleton through RhoA signaling inhibition 3, and activates epithelial-mesenchymal transition and STAT3 pathways. High GTPBP4 expression correlates with poor prognosis in HCC and CRC patients 4. Beyond cancer, GTPBP4 enhances developmental competence in prepubertal oocytes by promoting cell cycle progression and organelle maturation 5. Therapeutically, PKM2-specific inhibitors such as shikonin can suppress GTPBP4-driven HCC glycolytic reprogramming and tumor growth, offering a potential treatment strategy for HCC patients.