Cordycepin Induces Apoptosis and G2/M Phase Arrest through the ERK Pathways in Esophageal Cancer Cells

Esophageal cancer is one of the most aggressive and lethal gastrointestinal tract malignancies, with a poor overall five-year survival rate. Cordycepin, a major compound of Cordyceps sinensis, has been shown to have anticancer potential. This study focuses on the anticancer properties of cordycepin that target esophageal cancer and reveals molecular aspects underlying these effects. In our CCK-8 assays and colony formation assays, cordycepin significantly suppressed esophageal cancer cell proliferation. Moreover, cordycepin induced chromatin condensation in esophageal cancer cells and significantly increased the number of apoptotic cells through activation of caspase cascades, apoptotic signaling, and the regulation of Bcl-2 family members. Cell cycle assays showed that cordycepin altered cyclin-dependent kinase1 and cyclinB1 expression, which resulted in a G2/M phase blockade. Mechanistically, ERK pathway inactivation was involved in the anti-tumor functions of cordycepin. The same results were also observed in vivo. Taken together, these findings reveal that cordycepin induces pro-apoptosis and anti-proliferation mechanisms in cancer cells, and may represent a novel therapeutic agent.