Fig. 4

HIF-1-mediated cellular responses under normoxia. A HIF-1 contributes to metabolic reprogramming and the Warburg effect by encoding glucose transporters (GLUT1, GLUT3) and glycolytic enzymes (ALDOA, ENO1, GAPDH, HK1, HK2, PFKL, PGK1, PKM2, LDHA). B HIF-1 is involved in cellular metastasis through processes such as EMT, ECM remodeling, and tumor invasion. WDR5 and HDAC2 can enhance cell migration and invasion by stabilizing HIF-1α. Additionally, UCHL1 and USP14 maintain HIF-1α stability through their deubiquitination activity, promoting cellular migration. C HIF-1 plays a role in regulating the cell cycle, cell proliferation, and cell death: (i) in normoxia, the absence of p53 results in no checkpoint arrest, leading to normal proliferation; (ii) in pseudohypoxia, HIF-1α shortens the cell cycle independently of p53, as evidenced by reduced durations of various phases in the cycle, resulting in decreased cell proliferation; (iii) in hypoxia, p53 exerts its influence at the G1/S checkpoint, resulting in decreased cell proliferation