Inhibition of endogenous hydrogen sulfide production suppresses the growth of nasopharyngeal carcinoma cells

Abstract Hydrogen sulfide (H 2 S) has been widely recognized as one of gasotransmitters. Endogenous H 2 S plays a crucial role in the progression of cancer. However, the effect of endogenous H 2 S on the development of nasopharyngeal carcinoma (NPC) is still unknown. In this study, aminooxyacetic acid (AOAA, an inhibitor of cystathionine‐β‐synthase), dl ‐propargylglycine (PAG, an inhibitor of cystathionine‐γ‐lyase), and l ‐aspartic acid ( l ‐Asp, an inhibitor of 3‐mercaptopyruvate sulfurtransferase) were adopted to detect the role of endogenous H 2 S in NPC growth. The results indicated that the combine (PAG + AOAA + l ‐Asp) group had higher inhibitory effect on the growth of NPC cells than the PAG, AOAA, and l ‐Asp groups. There were similar trends in the levels of apoptosis and reactive oxygen species (ROS). In addition, the combine group exhibited lower levels of phospho (p)‐extracellular signal‐regulated protein kinase but higher expressions of p‐p38 and p‐c‐Jun N‐terminal kinase than those in the AOAA, PAG, and l ‐Asp groups. Furthermore, the combine group exerted more potent inhibitory effect on NPC xenograft tumor growth without obvious toxicity. In summary, suppression of endogenous H 2 S generation could dramatically inhibit NPC growth via the ROS/mitogen‐activated protein kinase pathway. Endogenous H 2 S may be a novel therapeutic target in human NPC cells. Effective inhibitors for H 2 S‐producing enzymes could be designed and developed for NPC treatment.