OTUD3-Mediated Deubiquitination Licenses TEX264 to Orchestrate ER-Phagy for KDM5B Degradation in Teniposide Lung Cancer Therapy - PubMed
4 hours ago
- #ER-Phagy
- #Lung Cancer
- #KDM5B Degradation
- High expression of KDM5B in lung cancer promotes tumorigenesis and immunosuppression.
- Teniposide (Ten) is identified as a potent anti-lung cancer agent that increases TEX264 stability.
- Teniposide suppresses lung cancer by degrading KDM5B through TEX264-associated ER-phagy.
- OTUD3, a deubiquitylase activated by Teniposide, stabilizes TEX264, facilitating ER-phagy.
- Genetic knockdown of TOP2A has minimal impact on Teniposide-mediated ER-phagy.
- Silencing OTUD3 reduces Teniposide-driven ER-phagy and KDM5B inhibition.
- Teniposide activates the immune microenvironment and inhibits lung cancer effectively.