Targeting TSPAN1 promotes ferroptosis in endometrial cancer cells, reduces energy metabolism and inhibits malignant behavior
This research endeavored to explore the significance of tetraspanin 1 (TSPAN1) in endometrial cancer, with a particular focus on its influence on ferroptosis and glycolytic activity. To achieve this, we established cell models that either overexpressed or silenced TSPAN1. We employed the CCK8 assay and EdU to assess the impact of TSPAN1 on cell proliferation. Additionally, scratch and Transwell assays were conducted to evaluate the cells' malignant biological behavior. The expression of ferroptosis-associated marker proteins was monitored. Further studies were conducted to investigate the effects of TSPAN1 on mitochondrial function, energy metabolism, and the cytoskeleton, and elucidated the interaction between TSPAN1 and SLC44A4. Our findings indicated that the downregulation of TSPAN1 markedly suppressed cell proliferation and the incidence of malignant biological behaviors. Moreover, the suppression of TSPAN1 was found to enhance ferroptosis and to reduce glycolytic activity. This study provides a comprehensive analysis of TSPAN1's role in endometrial cancer, shedding light on its potential as a key regulator of ferroptosis and glycolysis.