Conclusions
This study elucidated the mechanism of GluOC in inhibiting ferroptosis in TNBC. The findings not only provided new insights into ferroptosis but also potentially offered new concepts for the development of future anticancer therapies, which may contribute to improving the treatment of TNBC patients.
Methods
We screened out the differential genes related to ferroptosis in TNBC after GluOC treatment based on the whole-genome sequencing
Results
The results showed that GluOC enhanced glutathione expression levels by inducing SLC7A11 accumulation via the specific signaling pathway. Additionally, GluOC increased ATP production and tricarboxylic acid flux resistance to ferroptosis through SLC38A1. Overall, GluOC coordinately regulated SLC7A11 and SLC38A1 to inhibit ferroptosis in TNBC. Conclusions: This study elucidated the mechanism of GluOC in inhibiting ferroptosis in TNBC. The findings not only provided new insights into ferroptosis but also potentially offered new concepts for the development of future anticancer therapies, which may contribute to improving the treatment of TNBC patients.