The c-Myc-USP14-PFKP axis sustains chemoresistance in pancreatic ductal adenocarcinoma - PubMed
12 hours ago
- #metabolic reprogramming
- #chemoresistance
- #PDAC
- The c-Myc-USP14-PFKP axis plays a key role in sustaining chemoresistance in pancreatic ductal adenocarcinoma (PDAC).
- Metabolic reprogramming, particularly involving PFKP, a glycolytic enzyme, is linked to PDAC progression and drug resistance.
- Elevated PFKP expression correlates with poor patient survival and reduced sensitivity to gemcitabine-based chemotherapy.
- USP14 stabilizes PFKP through deubiquitination, while c-Myc transcriptionally upregulates USP14, forming a feed-forward regulatory circuit.
- Disrupting the c-Myc/USP14/PFKP axis enhances chemotherapy sensitivity in PDAC models.
- Combined targeting of PFKP and USP14 shows enhanced antitumor effects in various PDAC models.