Fig. 7: AMPK-PROX1 axis in human cancers is associated with patient prognosis.

a, b Representative IHC staining images (a) and statistical data (b) of p-S79 and p-AMPK expression in HCC tissues (n = 90). Scale bar, 500 µm. c Kaplan–Meier analysis of overall survival probability of p-S79 levels in HCC patients. The statistical significance was assessed using log-rank test according to HCC patients with low or high expression of p-S79. d Kaplan–Meier analysis of overall survival in the HCC patients (n = 90) according to combined expression status of p-S79 and p-AMPK. e, f Representative IHC staining images (e) and statistical data (f) of p-S79 and p-AMPK expression in lung adenocarcinoma (LUAD) tissues (n = 90). Scale bar, 500 µm. g, h Kaplan–Meier analysis of overall survival (g) and disease-free survival (h) probability of PROX1 levels in LUAD patients (n = 90). i, j Kaplan–Meier analysis of overall survival (i) and disease-free survival (j) probability of p-S79 levels in LUAD patients. k, l Kaplan–Meier analysis of overall survival (k) and disease-free survival (l) in NSCLC patients according to combined expression status of p-S79 and p-AMPK. m Glucose deprivation activated AMPK directly phosphorylated PROX1 at Ser79, allowing a rapid recruitment of Cul4-DDB1 E3 ubiquitin ligase complex to promote PROX1 degradation, a critical event that activates BCAA metabolism to suppress mTOR signalling pathway. Conversely, the deficient-LKB1-AMPK axis in cancers reactivates PROX1 to dictate BCAA catabolism and mTOR signalling, facilitating tumourigenesis and aggressiveness. For b and f, statistical significance was assessed using two-sided Chi-square test. Source data are provided as a Source Data file.