An elevated rate of glucose consumption and the dependency on aerobic glycolysis 
for ATP generation have long been observed in cancer cells, a phenomenon known 
as the Warburg effect. the altered energy metabolism in cancer cells provides an 
attractive opportunity for developing novel cancer therapeutic strategies. 
Lactate dehydrogenase (LDH), which catalyzes the transformation of pyruvate to 
lactate, plays a vital role in the process of glycolysis. It has been reported 
that the level of LDH-A expression is increased both in head and neck cancer 
cells and in the blood serum of nasopharyngeal carcinoma (NPC) patients, and is 
associated with poor prognosis. However, the effect of LDH-A inhibition on NPC 
cells remains unknown. Here, in the present study, we found that oxamate, a 
classical inhibitor of LDH-A, suppressed cell proliferation in a dose- and 
time-dependent manner both in CNE-1 and CNE-2 cells, two NPC cancer cell lines. 
LDH inhibition by oxamate induced G2/M cell cycle arrest via downregulation of 
the CDK1/cyclin B1 pathway and promoted apoptosis through enhancement of 
mitochondrial ROS generation. N-acetylcysteine, a specific scavenger of ROS, 
significantly blocked the growth inhibition effect induced by oxamate. We also 
identified that oxamate increased sensitivity to ionizing radiation in the two 
NPC cancer cell lines. Furthermore, we verified similar results in tumor 
xenograft models. collectively, these results suggest that LDH-A may serve as a 
promising therapeutic target for NPC treatment.