The MYBL2-GTSE1 axis promotes laryngeal squamous cell carcinoma progression by regulating PI3K/AKT-dependent glycolytic reprogramming - PubMed
4 hours ago
- #LSCC
- #Metabolic Reprogramming
- #PI3K/AKT
- MYBL2 is significantly overexpressed in laryngeal squamous cell carcinoma (LSCC) and correlates with poor prognosis.
- MYBL2 directly activates GTSE1 transcription, stimulating the PI3K/AKT signaling pathway.
- The MYBL2-GTSE1 axis upregulates glycolytic proteins (PKM2, HK2, GLUT1, LDHA), promoting metabolic reprogramming.
- This metabolic shift increases glycolysis (ECAR) and suppresses mitochondrial respiration (OCR).
- MYBL2 overexpression enhances LSCC cell proliferation, migration, and invasion in vitro and tumor growth in vivo.
- GTSE1 knockdown or PI3K inhibition (LY294002) reverses the oncogenic effects of MYBL2.
- The MYBL2-GTSE1 axis is a promising therapeutic target for LSCC.