Gene BDH2 suppresses lung cancer spread by triggering iron-dependent cell death.
BDH2 overexpression in LUAD cell lines and xenograft mice significantly inhibited migration, invasion, and metastasis. Mechanism: BDH2 suppresses the Nrf2/HO-1 ferroptosis-resistance pathway, enhancing cancer cell sensitivity to ferroptotic death. Ferroptosis inhibitor Fer-1 reversed these effects,…
Gene BDH2 suppresses lung cancer spread by triggering iron-dependent cell death.
BDH2 overexpression in LUAD cell lines and xenograft mice significantly inhibited migration, invasion, and metastasis. Mechanism: BDH2 suppresses the Nrf2/HO-1 ferroptosis-resistance pathway, enhancing cancer cell sensitivity to ferroptotic death. Ferroptosis inhibitor Fer-1 reversed these effects, confirming ferroptosis as the key mechanism.
Key Findings
- BDH2 overexpression inhibited LUAD cell migration and invasion in vitro
- In vivo: BDH2 reduced tumor growth and metastasis in xenograft mice
- BDH2 suppresses Nrf2/HO-1 pathway, enhancing ferroptosis sensitivity
- Ferroptosis inhibitor Fer-1 reversed anti-metastatic effects
- BDH2 identified as a potential therapeutic target for LUAD
Implications
BDH2-mediated ferroptosis represents a new avenue for metastatic LUAD treatment. Drugs enhancing BDH2 activity or activating ferroptosis independently could be combined with existing therapies.
Caveats
Preclinical cell line and xenograft study; abstract-only. Nrf2/HO-1 inhibition has broad cellular effects. Significant translational gap.
Source: Archivum immunologiae et therapiae experimentalis — 2026-01-01