Targeting ACSS2 disrupts metabolic-epigenetic crosstalk to restore apoptosis and temozolomide chemosensitivity in pancreatic neuroendocrine tumors - PubMed
4 days ago
- #ACSS2
- #PNETs
- #Chemoresistance
- Targeting ACSS2 disrupts metabolic-epigenetic crosstalk to restore apoptosis and TMZ chemosensitivity in PNETs.
- ACSS2 is upregulated in PNETs and correlates with chemoresistance by promoting histone hyperacetylation and BCL6 transcription.
- BCL6 silences TP53, bypassing TMZ-induced G2/M arrest and suppressing apoptosis.
- Inhibition of the ACSS2/BCL6 axis restores P53-mediated DNA damage response and TMZ sensitivity.
- Combined ACSS2 inhibition and anti-PD1/L1 immunotherapy shows superior efficacy in PNET models.