Bis-type Triaziquone Induces Apoptotic Effects in Human OEC-M1 Oral Cancer Cells

Oral cancer is a major global public health concern. Despite advancements in treatment, the 5-year survival rate for patients with oral cancer remains low. Developing new therapies or drugs is essential for improving patient outcomes. This study aimed to evaluate the anticancer effects of bis-type triaziquone (BTZQ), a synthesized chemical compound, in an oral cancer cell line.

The oral cancer cell line OEC-M1 and oral fibroblast (OF) cells were used in this study. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, propidium iodide staining, and immunoblotting assays were performed to assess cell viability, DNA fragmentation, and protein expression, respectively.

MTT assays showed that BTZQ significantly reduced OEC-M1 cell viability, with OEC-M1 cells being more sensitive to BTZQ than OF cells. Additionally, BTZQ increased the percentage of OEC-M1 cells in the subG1 phase and induced PARP cleavage, both indicators of apoptosis. Furthermore, BTZQ activated the expression of initiator caspases (caspase-8 and caspase-9) and effector caspases (caspase-3 and caspase-7) in OEC-M1 cells. Furthermore, treatment with BTZQ significantly induced DNA damage, NF-κB activation, and Fas expression.

BTZQ effectively reduces the viability of OEC-M1 cells, showing greater toxicity to them compared to normal OF cells. It also induces several apoptotic features, including an increased subG1 phase population, PARP cleavage, and caspase activation in OEC-M1 cells, highlighting its potential as an oral cancer therapeutic by promoting apoptosis.