Glioblastoma multiforme is a
malignant neoplasm of the brain with poor prognosis. The first-line drug against
glioblastoma is the
alkylating agent temozolamide (TMZ); unfortunately, treatment resistance and
tumor re-incidence are common. In some cases, immunogenic cell death (ICD) inducers can decrease treatment resistance and
tumor recurrence by stimulating an antitumor specific immune response. Not all ICD inducers, however, are suitable for
glioma patients because of the low permeability of the blood-brain barrier (BBB).
Panobinostat (PAN), a
histone deacetylase inhibitor and Lophophora williamsii (LW) extract can pass through the BBB and have antitumor properties. The aim of this study is to evaluate the cytotoxic potential of TMZ, PAN and LW extract against the
glioma C6 cell line, and its role in the release of damage-associated molecular patterns (DAMPs), which is a hallmark of ICD. Our results indicate that all treatments induce cellular death in a time- and concentration-dependent manner, and that PAN and LW extract induce apoptosis, whereas TMZ induces apoptosis and
necrosis. Also, that some of the treatments and their sequential administration induce the release of DAMPs. Furthermore, in a rat
glioma model, we observed that all treatments decreased
tumor volume, but the in vivo cell death mechanism was not ICD. Our findings indicate that TMZ, PAN, and LW combination have a cytotoxic effect against
glioma cells but do not induce ICD.