Caspase-3/-9 as tongue cancer cell apoptosis target induced by ibuprofen

Background: Tongue carcinoma is different from oral cancer in other areas because it has a high amount of cell growth, localized migration, and a higher rate of spreading to cervical lymphatic nodes. Therapeutic alternatives, particularly concerning recurrent malignancies, are notably constrained. Nevertheless, it is imperative to explore novel methodologies for refractory neoplasms, one of which may involve the application of ibuprofen. Purpose: The goal of this study was to look at how well caspase-3 and -9 break down proteins as possible targets for apoptosis in tongue cancer cells that were caused by ibuprofen. Methods: A controlled laboratory experiment employing a post-test-only design was executed. We used a colorimetric test for caspase-3 and -9 to check for the induction of apoptosis. The suppression of cellular invasion was verified through the Boyden chamber assay. Western blot analysis was utilized to identify the presence of caspase-3 and -9 proteins. The administered doses of ibuprofen were calibrated at 0, 5, 10, 25, 50, and 100 µg/mL. Data were subjected to analysis using two-way ANOVA followed by post-hoc Least Significant Different (LSD), with a significance threshold set at 95%. Results: It was established that ibuprofen at dosages ranging from 25 to 100 µg/mL significantly facilitated apoptosis in cells through an augmentation of the proteolytic activity of caspase-3 and -9. Notably, caspase-9 exhibited a superior proteolytic activity (1.85-fold) compared to caspase-3 (1.30-fold) (P = 0.038) at the 100 µg/mL concentration. The upregulation of caspase-3 and -9 proteins was observed in cells treated with ibuprofen. Ultimately, ibuprofen demonstrated an ability to inhibit the invasion of tongue carcinoma cells across various dosages. Conclusion: Ibuprofen has been shown to induce the proteolytic activities of caspase-3 and -9 in tongue carcinoma cells. However, the proteolytic activity of caspase-9 surpassed that of caspase-3, suggesting that targeting this protein may constitute a promising novel therapeutic strategy for this cancer variant.