OBJECTIVETo evaluate apoptotic effects of cisplatin and cordycepin as single agent or in combination with cytotoxicity in oral cancer cells.

METHODSThe influences of cisplatin (2.5 μg/mL) and/or cordycepin treatment (10 or 100 μmol/L) to human OC3 oral cancer cell line were investigated by morphological observation for cell death appearance, methylthiazoletetrazolium (MTT) assay for cell viability, flow cytometry assay for cell apoptosis, and Western blotting for apoptotic protein expressions.

RESULTSData demonstrated that co-administration of cisplatin (2.5 μg/mL) and cordycepin (10 or 100 μmol/L) resulted in the enhancement of OC3 cell apoptosis compared to cisplatin or cordycepin alone treatment (24 h), respectively (P <0.05). In flow cytometry assay, percentage of cells arrested at subG1 phase with co-treatment of cordycepin and cisplatin (30%) was significantly higher than cisplatin (5%) or cordycepin (12%) alone group (P <0.05), confirming a synergistically apoptotic effect of cordycepin and cisplatin. In cellular mechanism study, co-treatment of cordycepin and cisplatin induced more stress-activated protein kinase/Jun terminal kinase (JNK), the expressions of caspase-7, and the cleavage of poly ADP-ribose polymerase (PARP) as compared to cisplatin or cordycepin alone treatment (P <0.05).

CONCLUSIONCisplatin and cordycepin possess synergistically apoptotic effect through the activation of JNK/caspase-7/PARP pathway in human OC3 oral cancer cell line.

Apoptosis ; drug effects ; Caspase 7 ; metabolism ; Cell Count ; Cell Line, Tumor ; Cell Shape ; drug effects ; Cell Survival ; drug effects ; Cisplatin ; pharmacology ; Deoxyadenosines ; pharmacology ; Drug Synergism ; G1 Phase ; drug effects ; Humans ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Mouth Neoplasms ; pathology ; Phosphorylation ; drug effects ; Poly(ADP-ribose) Polymerases ; metabolism