KDM5C-regulated SIX5 promotes glioblastoma progression through transcriptional activation of UBE2C and enhancement of the Warburg effect - PubMed
6 hours ago
- #Transcriptional Regulation
- #Warburg Effect
- #Glioblastoma
- SIX5 is highly expressed in glioblastoma (GBM) and associated with poor prognosis.
- KDM5C positively regulates SIX5, which transcriptionally activates UBE2C.
- SIX5 promotes GBM progression via UBE2C-mediated AKT/mTOR signaling and enhancement of aerobic glycolysis (Warburg effect).
- Knockdown of SIX5 inhibits GBM cell proliferation, migration, invasion, and tumorigenicity, while promoting apoptosis.
- UBE2C overexpression partially rescues malignant phenotypes under SIX5 downregulation, confirming the axis role.
- The KDM5C-SIX5 - UBE2C axis is validated in vivo as a driver of GBM growth and represents a potential therapeutic target.