NSUN2-FOSB reciprocity facilitates leukemogenesis in an m5C-dependent manner by increasing BCL2L1 expression - PubMed
a day ago
- #AML
- #RNA methylation
- #leukemogenesis
- NSUN2 is upregulated in AML patient samples compared to normal hematopoietic cells.
- NSUN2 knockdown impairs AML cell proliferation, induces apoptosis, and reduces colony formation.
- Genetic ablation of NSUN2 in a murine AML model impairs leukemia stem cell self-renewal and prolongs survival.
- NSUN2's effects on leukemogenesis are dependent on its catalytic activity for m5C RNA modification.
- NSUN2 stabilizes FOSB mRNA via m5C modification, leading to increased FOSB expression.
- FOSB transcriptionally activates NSUN2, creating a feedforward regulatory loop.
- FOSB promotes BCL2L1 expression by binding to its promoter, enhancing anti-apoptotic effects.
- The NSUN2-FOSB-BCL2L1 axis is identified as a key driver of AML leukemogenesis in an m5C-dependent manner.