Pterostilbene suppresses the growth of esophageal squamous cell carcinoma by inhibiting glycolysis and PKM2/STAT3/c-MYC signaling pathway.

Pterostilbene (PTS) is a dietary phytochemical that has shown antitumor activity in many types of cancer, but the molecular mechanism remains unclear. It has also not been adequately studied on PTS against esophageal squamous cell carcinoma (ESCC). Thus, this study investigated the effect of PTS on ESCC in vitro and in vivo and explored the underlying molecular mechanism. We found that PTS can inhibit the proliferation, colony formation, and migration of ESCC cells. According to the bioinformatics analysis of proteomics, PTS had a great influence on the metabolic process of ESCC cells. KEGG analysis showed that PTS down-regulated the pyruvate metabolism pathway. Moreover, PTS can inhibit the PK activity, glucose consumption, and lactate production in ESCC cells. By administration of PTS into xenograft mice, experiment results demonstrated that PTS can suppress tumor progress and the PKM2/STAT3/c-MYC signaling pathway. We found that PTS inhibited the PKM2/STAT3/c-MYC signaling pathway by targeting PKM2 in ESCC cells. Collectively, this study revealed that PTS inhibited ESCC growth by suppressing PKM2 mediated aerobic glycolysis and PKM2/STAT3/c-MYC signaling pathway, which enriching the anti-tumor molecular mechanism of PTS and providing a theoretical basis for its clinical application.