Reply to correspondence 1 on “MET promotes hepatocellular carcinoma development through the promotion of TRIB3-mediated FOXO1 degradation”

I would like to express my appreciation to Tiantian Wang, Wenjie Huang and Limin Xia for their Correspondence [1,2] as a reply to my editorial entitled “Unveiling TRIB3: A New Mediator in MET-Driven Hepatocellular Carcinoma Progression” [3]. As a cancer researcher focused on basic liver cancer research, I found their insights particularly engaging. The exploration of TRIB3’s role in hepatocellular carcinoma (HCC) across different etiologies, including hepatitis B virus-related HCC and non-alcoholic steatohepatitis-related HCC, is indeed intriguing. Utilizing alpha-fold predictions to identify the molecular interactions between TRIB3 and COP1 may present a promising avenue for research. Based on this analysis, the authors may develop a therapeutic peptide [4] with the goal to disrupt the interaction between these proteins, thereby confirming their functional interplay. I believe the proposed future directions will provide a more comprehensive understanding of the role of TRIB3 in HCC. I would like to conclude this Reply by expressing my gratitude to the responses of Wang and the colleagues for providing further characterization, future perspectives and therapeutic implications for the role of TRIB3 in HCC.