“…In addition, HIF1α has been associated with the activation of Ror1 transcription to influence cancer progression [ 18 ], and it regulates miR-210-3p, CXCR7, CXCR4, IDH1, C-Met, SF/HGF, the S100A4/NMIIA axis, NO, VEGF, BAG3, and TDO2, and influences various aspects of the glioblastoma biology such as angiogenesis, invasion, metabolism and therapy resistance [ 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 30 , 31 , 32 , 33 , 34 ]. Similarly, HIF2α has been shown to regulate GPx1 to ensure resistance to oxidative stress and radiation [ 59 ], while contributing to glioblastoma progression via various mechanisms such as the DDX28-mediated regulation of eIF4E2-driven translation [ 49 ]. In addition, other factors such as miR-370-3p [ 61 ], NIX-mediated mitophagy [ 62 ], and p21 (CDKN1A)[ 63 ] have been identified as crucial players in glioblastoma pathogenesis, highlighting the complex interplay of genetic alterations in shaping the aggressive behavior of glioblastoma cells in the hypoxic tumor microenvironment.…”