Notably, the administration of exogenous recombinant ENO1 (rhENO1) effectively mitigated the proliferative and invasive deficits in ENO1-knockdown GBM cells, indicating extracellular activity independent of intracellular glycolytic functions, likely mediated by autocrine/paracrine signaling via cell-surface receptors. Here, ENO1 is linked to glioblastoma.