CHK2 is involved in the p53-independent radiosensitizing effects of valproic acid

摘要: Radiotherapy is an effective treatment for the majority of types localized solid cancer. However, risk side effects to surrounding normal tissues limits radiotherapeutic approaches. Whilst mechanism action valproic acid, inhibitor histone deacetylase, remains unknown, a potential antineoplastic radiosensitizer. The present study demonstrated in vitro radiosensitizing acid on human breast cancer MCF7 cell line, and revealed that increased level DNA breakage, apoptosis senescence. In addition, western blot analyses induced tumor suppressor protein (p)53 p21 expression, activated checkpoint kinase 2 (CHK2) cells primary mouse embryonic fibroblasts. Notably, with also increases levels CHK2 activity p53-null colon HCT116 cells. Furthermore, acid-induced radiosensitization was largely dependent CHK2. results reveal may exhibit clinical utility respect increasing anticancer efficacy radiotherapy by affecting p53.