β-Asarone suppresses TGF-β/Smad signaling to reduce the invasive properties in esophageal squamous cancer cells

Esophageal cancer is one of the most common malignancies which induces cancer-related death. Cancer metastasis and recurrence are the main obstacle faced in esophageal cancer treatment. beta-Asarone has been shown to act as an anti-cancer reagent in various cancer types. However, the anti-cancer activities of beta-Asarone in esophageal cancer have not been shown. In the current study, we show that beta-Asarone suppressed the proliferation of esophageal squamous cancer cells (ESCC) in both dose- and time-dependent manners. Moreover, beta-Asarone treatment increases activated caspase 3, caspase 9, and cleaved poly ADP-ribose polymerase, and induces apoptosis in ESCC. Additionally, beta-Asarone also suppresses epithelial-mesenchymal transition (EMT) and the invasive and migratory abilities in ESCC. Interestingly, beta-Asarone suppresses TGF-beta/Smad signaling by inhibition of TGF-beta-induced phosphorylation of Smad2 and Smad3. Importantly, we show that inhibition of TGF-beta/Smad signaling activation is critical for beta-Asarone-suppressed EMT. Our data revealed a novel role of beta-Asarone which targets invasive properties by inhibiting TGF-beta/Smad signaling activation in ESCC. Our study suggests the potential application of beta-Asarone to reduce cancer metastasis and recurrence in esophageal cancer treatment.

Automated summary

This study found that beta-Asarone can inhibit the proliferation and induce apoptosis in esophageal squamous cell carcinoma (ESCC). Additionally, beta-Asarone also suppresses epithelial-mesenchymal transition (EMT) and invasive abilities in ESCC. The study also discovered that beta-Asarone inhibits TGF-beta/Smad signaling activation to suppress invasive properties in ESCC.