肝细胞癌
生物
转移
丝氨酸
癌症研究
基因
计算生物学
遗传学
癌症
磷酸化
作者
Hongwei Cui,Jiang Li,Yujiao Zhou,You Zhou,Fan Li,Zhenzhen Zhang
标识
DOI:10.1007/s10142-024-01497-7
摘要
Metastasis is responsible for approximately 90% of lethality from solid tumors. Metabolic abnormalities are one of the key characteristics of tumor cells, closely associated with tumorigenesis and progression. The de novo synthesis pathway of serine is a key metabolic bypass in glycolysis, which could provide material and energy basis for the rapid proliferation of tumor cells by mediating one-carbon metabolism. The transformation of metabolic patterns is particularly pronounced in HCC, often leading to a high dependence of HCC cells on glycolysis. However, up to now, the underlying relationship between serine metabolism and HCC metastasis remains largely unknown. Through a series of bioinformatics methods, we reported CCT6A, a serine related gene, was particularly associated with metastatic events of HCC. We furtherly demonstrated that CCT6A was highly expressed in HCC cells with high metastatic potential. Gain- and loss-of-function analyses showed that CCT6A could promote HCC cells migration and invasion. Mechanistically, CCT6A was found to be interacted with RPS3, and might potentiate the metastasis of HCC by affecting some metabolic processes. Totally, our results suggest that the metabolic reprogramming induced by interacting between CCT6A and RPS3 could advance HCC metastasis, making the CCT6A/RPS3 axis a promising target for therapeutic intervention.
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