Capsaicin inhibits glycolysis in esophageal squamous cell carcinoma by regulating hexokinase‑2 expression.

Capsaicin is a principal component of hot red peppers and chili peppers. Previous studies have reported that capsaicin exhibits antitumor functions in a variety of tumor models. Although various mechanisms underlying the capsaicin‑mediated inhibition of tumor growth have been demonstrated, the impact of capsaicin on tumor metabolism has rarely been reported. The present study demonstrated that capsaicin exhibited an inhibitory effect on tumor glycolysis in esophageal squamous cell carcinoma (ESCC) cells. Following treatment with capsaicin, glucose consumption and lactate production in ESCC cells was decreased. Capsaicin resulted in a decrease of hexokinase‑2 (HK‑2) expression, which is known for its important role in tumor glycolysis. Further investigations demonstrated that phosphatase and tensin homolog (PTEN) expression was increased in ESCC cells treated with capsaicin, and that the RAC‑α serine threonine‑protein kinase signaling pathway was downregulated. In PTEN‑knockdown KYSE150 cells, the decrease in HK‑2 and inhibition of glycolysis caused by capsaicin was attenuated, which suggested that the impact of capsaicin on tumor metabolism was associated with its effect on PTEN.