Exploring the Cytotoxic and Anticancer Potential of Naringin on Oral Cancer Cell Line.

Introduction Oral cancer is the most persistent, aggressive primary malignant sarcoma that is globally prevalent. Though chemotherapy is the only treatment option, it has not progressed for years to overcome its detrimental side effects. Introducing novel therapeutic techniques to improve effectiveness is the need of the hour. Aim This study aimed to investigate the pro-apoptotic effects of naringin in oral cancer cell lines. Methodology The cell viability of oral cancer cells treated with naringin was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. Naringin was given to oral cancer cells (KB-1) in concentrations ranging from 20 to 200 µM/mL for 24 hours. A phase-contrast microscope is used to examine cell morphology changes. Ethidium bromide (EtBr) staining was employed to study nuclear morphological alterations in oral cancer cells. The apoptotic nuclei were viewed under a fluorescent microscope. To determine pro-apoptotic levels, quantitative real-time polymerase chain reaction (PCR) gene expression analysis was performed to evaluate the expression of transforming growth factor-beta (TGF-β), suppressor of mothers against decapentaplegic 2 (SMAD2), tumor necrosis factor alpha (TNFα), and nuclear factor kappa B (NFκB). A scratch wound healing experiment was used to evaluate naringin's anti-migratory properties. Results Our study found that naringin treatment significantly reduced cell viability in oral cancer cells compared to the control group (p < 0.05). In oral cancer cells, we found an inhibitory concentration (IC) of 125.3 μM/mL. Following treatment, fewer cells were present, and those that were present shrunk and displayed cytoplasmic membrane blebbing. The EtBr staining reveals chromatin condensation and nuclear breakage in treated cells. The study found that naringin downregulates the expression of B-cell leukemia/lymphoma 2 (Bcl-2), TGF-β, SMAD2, TNFα, and NFκB and upregulates the expression of Bcl-2-associated agonist of cell death (BAD), Bcl-2-associated protein X (BAX), and caspase-3. Furthermore, when compared to control cells, naringin significantly reduced cell migration. Naringin treatment significantly promotes apoptosis and inhibits migration by altering the SMAD2 signaling pathway. Conclusion Overall, this study highlights the promising role of naringin as a pro-apoptotic and cytotoxic phytochemical regulating the gene expression of Bcl-2, TGF-β, SMAD2, TNFα, NFκB, BAD, BAX, and caspase-3, thereby treating oral cancer.