Increasing radiation sensitivity in esophageal cancer by blocking polo-like kinase 1

Volasertib significantly enhanced radiation-induced death in esophageal cancer cells.

• PLK1 inhibition decreased the proliferation of esophageal cancer cells in a dose- and time-dependent manner.
• The combination of volasertib and radiation caused G2/M cell cycle arrest and increased levels of cyclin B.
• Apoptosis was induced in esophageal cancer cells when treated with both volasertib and irradiation.
• Volasertib treatment improved local tumor control in animal models compared to either treatment alone.
• Results suggest that targeting PLK1 may improve the efficacy of radiation therapy in esophageal cancer.

Simplified