Inhibition of centrosomal protein 164 sensitizes rhabdomyosarcoma cells to radiotherapy.

Rhabdomyosarcoma is the second most common malignant tumor of the heart in infants and children and cannot often be resected completely. Chemotherapy and radiotherapy have a critical role in relieving symptoms and prolonging survival; therefore, enhancing the sensitivity of rhabdomyosarcoma to radiotherapy is an important area of investigation in order to improve the prognosis of patients. It has been reported that centrosomal protein 164 (CEP164) has a key role in the DNA damage-activated signaling cascade. CEP164 is often overexpressed in tumors and is associated with poor prognosis in various types of cancer. In the present study, the influence of CEP164 on the radiosensitivity of rhabdomyosarcoma cells was investigated. Results demonstrated that CEP164 is involved in the radiation-induced cellular response. CEP164 is increased upon radiation and influences the cell cycle, cell viability and cell apoptosis. CEP164 depletion enhanced cellular sensitivity to radiation, promoted cell apoptosis, decreased cell viability and induced gap 2/mitosis arrest of the cell cycle. The present study identified the function of CEP164 in radiation resistance in rhabdomyosarcoma, providing a potential therapeutic target for rhabdomyosarcoma treatment by disrupting CEP164.