Targeting UGCG sensitizes AML cells to venetoclax through RAB32-mediated endoplasmic reticulum-mitochondria communication - PubMed
5 hours ago
- #venetoclax
- #AML
- #UGCG
- Targeting UGCG sensitizes AML cells to venetoclax by promoting apoptosis and reducing cell viability.
- Inhibition of UGCG, either genetically or with eliglustat, suppresses AML cell growth effectively.
- Combination therapy (eliglustat + venetoclax) induces ceramide accumulation, activating ER stress (GRP78/PERK/CHOP axis).
- RAB32 activation leads to mitochondrial fission via ER-mitochondria communication and DRP1 activation.
- This strategy offers a potential alternative treatment for AML by leveraging ceramide-mediated cell death.