Capsaicin Promotes Apoptosis and Inhibits Cell Migration via the Tumor Necrosis Factor-Alpha (TNFα) and Nuclear Factor Kappa B (NFκB) Signaling Pathway in Oral Cancer Cells.

Background Oral squamous cell carcinoma (OSCC) is a highly prevalent cancer worldwide. Microbial infections, poor oral hygiene, and chronic viral infections such as human papillomavirus (HPV) contribute to its incidence. Capsaicin, known for its presence in chili peppers, has demonstrated potential antiproliferative effects in cancer cells. It operates by inducing programmed cell death, regulating the expression of transcription factors, halting cell cycle progression, and influencing growth signal transduction pathways. These findings suggest capsaicin's promising role as a candidate for further exploration in combating oral cancer. Aim This study intends to identify and evaluate the anticancer properties of capsaicin on oral cancer cells through in vitro investigations. Methodology Using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) technique, the cell viability of oral cancer cells treated with capsaicin was evaluated. Capsaicin was applied to the KB1 cells in a range of concentrations (25-150 µg/mL) over 24 hours. The morphological alterations of the cells were assessed using a phase contrast microscope. Nuclear factor kappa B (NFκB) and tumor necrosis factor-alpha (TNFα) were subjected to quantitative real-time polymerase chain reaction (PCR) gene expression analysis. To investigate nuclear morphological changes, oral cancer cells were stained with acridine orange/ethidium bromide (AO/EtBr). The apoptotic nuclei were visualized using a fluorescent microscope. A scratch wound healing test was performed to check for capsaicin's anti-migratory potential. Result In our investigation of oral cancer cells treated with capsaicin, there was a significant drop in cell viability between the control and treatment groups (p < 0.05). The inhibitory concentration (IC50) was found to be 74.4 μM/mL in oral cancer cells. Following treatment, fewer cells were present, and those that were present shriveled and exhibited cytoplasmic membrane blebbing. Under AO/EtBr staining, treated cells exhibited chromatin condensation and nuclear disintegration. Furthermore, the migration of capsaicin-treated cells was significantly lower than that of control cells. The results of gene expression analysis demonstrated a considerable downregulation of TNFα and NFκB following capsaicin administration. Conclusion The study's findings suggest that capsaicin may have anti-tumor properties in oral cancer cells. More research is desperately needed to fully understand the mechanism underlying capsaicin's anticancer potential and therapeutic applicability.