In our research, we discovered that the gluconeogenic enzyme FBP1 acts as a crucial p53 target, whose elevation is often suppressed in human HCC, suggesting a significant role in tumorigenesis.
The study highlights that elevated levels of metabolic stress-related signals activate pathways that lead to the degradation of tumor suppressors, linking metabolic dysfunction with oncogenesis in hepatocytes.
Our findings indicate that the dual regulation of FBP1 by AKT and NRF2 signifies a complex interplay between metabolic signals and oncogenic pathways that can drive HCC evolution.
By understanding the mechanisms through which metabolic dysfunction and cellular senescence impact HCC, we pave the way for potential therapeutic strategies aimed at reversing these detrimental processes.
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