Summary
Published in Cell & Bioscience (2025), this peer-reviewed study used 3D Petri Dish® micro-molds to form scaffold-free 3D microtissues. Full citation: Ma, Xiang, et al. The HNRNPC/CELF2 signaling pathway drives glycolytic reprogramming and mitochondrial dysfunction in drug-resistant acute myeloid leukemia
The HNRNPC/CELF2 signaling pathway drives glycolytic reprogramming and mitochondrial dysfunction in drug-resistant acute myeloid leukemia
Research Overview
Acute myeloid leukemia resists treatment in part through metabolic reprogramming. This study investigated the HNRNPC/CELF2 signaling pathway and its role in leukemia cell metabolism and drug resistance.
HNRNPC was found to regulate CELF2 expression through m6A modification. Drug-resistant leukemia cells showed increased HNRNPC and decreased CELF2, accompanied by upregulated glycolysis, higher glucose consumption, more lactate production, and mitochondrial dysfunction. Knocking down HNRNPC reduced both glycolysis and cell invasion, identifying the axis as a metabolic driver of resistance.
Key Discoveries
- HNRNPC regulates CELF2 via m6A modification in acute myeloid leukemia
- Drug-resistant cells showed elevated glycolysis, lactate production, and mitochondrial dysfunction
- HNRNPC knockdown reduced glycolysis and invasion, suggesting a therapeutic target
