Theaflavin-Induced Apoptosis in Oral Cancer Cells via Caspase-Mediated Mitochondrial Pathway

Background: Oral cancer remains a significant global health burden with high morbidity and mortality. Resistance to apoptosis is a major challenge in cancer therapy. Natural compounds such as Theaflavin, a polyphenol found in black tea, have shown potential anticancer properties. This study investigates the apoptotic effects of Theaflavin on KB human oral carcinoma cells. Objectives: To evaluate the cytotoxic and apoptosis-inducing potential of Theaflavin in KB cells through morphological assessment and gene expression analysis of caspase pathway markers. Methods: KB cells were treated with Theaflavin at 1, 10, 25, 50, and 100 µg/mL concentrations. Doxorubicin (1 µg/mL) served as the positive control, and untreated cells as the negative control. Cell viability was assessed using the MTT assay. Apoptosis was evaluated by morphological observation and qRT-PCR analysis of Bax, Bcl-2, Caspase-3, Caspase-9, and PARP1 expression. Results: Theaflavin induced a dose-dependent reduction in cell viability and morphological changes consistent with apoptosis, including cell shrinkage and fragmentation. Gene expression analysis revealed upregulation of pro-apoptotic markers (Bax, Caspase-3, Caspase-9, PARP1) and downregulation of Bcl-2, confirming activation of the intrinsic apoptotic pathway. Conclusion: Theaflavin effectively induces apoptosis in KB oral cancer cells through caspase-mediated mitochondrial pathways. It holds promise as a natural anticancer agent and warrants further investigation in preclinical models.