ENO1 influences ATP pool of cytoplasm and lactate homeostasis by regulating glycolysis to promote tumor stemness and metastasis
This study demonstrated the role of the glycolytic enzyme alpha-enolase (ENO1) on glycolysis and stemness in gastric cancer (GC). High ENO1 expression was associated with poor prognosis and promoted malignant phenotypes and stem-like characteristics in GC. Mechanistically, ENO1 directly stimulated lactate and ATP production by regulating glycolysis, affecting lactate homeostasis and intracellular ATP pools, and co-regulating the AMPK/mTOR and PI3K/AKT signaling pathways. This ultimately drove GC stemness, epithelial-mesenchymal transition (EMT)-related markers, self-renewal, migration, and invasion. Overall design: This submission contains RNA-Sequencing data from gastric cancer cell lines designed to investigate the transcriptional changes resulting from ENO1 (alpha-enolase) knockdown. The dataset includes three biological replicates of ENO1-knockdown cells (shENO1) and three biological replicates of control cells transfected with non-targeting shRNA (shCON).