Abstract
Metabolism reprogramming and excessive glycolysis are associated with rapid cancer cell growth, motility, and resistance to drug treatment. Therefore, identifying candidates for regulating the ratio of glycolysis and gluconeogenesis is a priority. Especially the reverse effect of Aldolase/Fructose‐1,6‐Bisphosphatase. Fructose‐1, 6‐bisphosphate (F‐1,6‐BP), is a vital intermediate involvement in glucose metabolism. When F‐1,6‐BP is converted into the 3‐carbon product by Aldolase, the glycolysis will proceed sequentially, while FBP1 can reverse the equation. Based on established immunoprecipitation and proteomic analyses revealed several candidates, including the anterior gradient 2 (AGR2), ubiquitin ligase gene cullin 4B (CUL4B), and telomeric repeat binding factor 1 (TERF1) that significantly modulates the ratio between ALDOA and FBP1. Our study demonstrated the inversed correlation of ALDOA and FBP1 associated with lung adenocarcinoma and hepatocellular carcinoma progression. Molecular simulated analysis and clinical correlation indicated that CUL4B is the novel factor in switching ALDOA and FBP1. Moreover, we evaluate the CUL4B‐relative glucose metabolism events to describe how CUL4B participates in the switch of ALDOA and FBP1. Based on these relationships, we claimed that CUL4B could trigger glucose metabolism reprogramming and be used as a therapeutic target for further research.
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