APR-246 combined with 3-deazaneplanocin A, panobinostat or temozolomide reduces clonogenicity and induces apoptosis in glioblastoma cells

Glioblastoma is the most malignant brain tumor and presents high resistance to chemotherapy radiotherapy. Surgery, radiotherapy with temozolomide are only treatments against this tumor. New targeted therapies, including epigenetic modulators such as 3‑deazaneplanocin A (DZ‑Nep; an EZH2 inhibitor) panobinostat (a histone deacetylase being tested in vitro, together temozolomide. The present study combined APR‑246 DZ‑Nep, teomozolomide order explore possibility of restoring p53 function mutated cases glioblastoma. Following Chou‑Talalay method it was demonstrated that acts additive manner other compounds, reducing clonogenicity inducing apoptosis glioblastoma cells independently status.