Lactate Dehydrogenase B delactylation promotes gastric cancer metastasis via enhancing glutathione-mediated resistance to ferroptosis | Synapse
March 2, 2026Open Access
Lactate Dehydrogenase B delactylation promotes gastric cancer metastasis via enhancing glutathione-mediated resistance to ferroptosis
Key Points
This research aims to understand how LDHB-K58 delactylation contributes to gastric cancer metastasis and resistance to treatment.
Investigated the role of LDHB-K58 delactylation in gastric cancer cells.
Analyzed SLC7A11-mediated GSH synthesis and its relation to ferroptosis resistance.
Utilized experimental models to observe metastasis rates in response to delactylation.
Delactylation of LDHB enhances GSH synthesis, promoting ferroptosis resistance.
Increased metastasis observed in gastric cancer models due to elevated ferroptosis resistance.
Targeting this metabolic pathway shows potential as a therapeutic strategy.
Abstract
LDHB-K58 delactylation drives gastric cancer metastasis via SLC7A11-mediated GSH synthesis and ferroptosis resistance, suggesting therapeutic targeting of this axis for overcoming therapy resistance.