Lactate-induced miR-7-5p/TRIM33 Reprograms Metabolic Flux to Suppress Tumor Growth and Viral Reactivation - PubMed
5 hours ago
- #metabolic reprogramming
- #EBV-associated cancers
- #lactate signaling
- Lactate-induced miR-7-5p/TRIM33 plays a role in metabolic reprogramming to suppress tumor growth and viral reactivation.
- Lactate-driven acidosis in the tumor microenvironment (TME) promotes tumor progression and supports Epstein-Barr virus (EBV) activity.
- miR-7-5p is identified as a lactate-downregulated microRNA with diagnostic potential in EBV-associated cancers like DLBCL and NPC.
- TRIM33, a lactate-inducible transcriptional regulator, is directly targeted by miR-7-5p and influences glycolytic gene expression.
- Lactate enhances TRIM33 binding to glycolytic gene promoters, such as SLC16A1 (MCT1), altering metabolic flux.
- Loss of TRIM33 accelerates tumor growth, increases EBV reactivation, and reduces sensitivity to lactate-transporter inhibitors.
- The study suggests circulating miR-7-5p as a noninvasive biomarker and TRIM33 as a therapeutic target for dual intervention.