Effects Of Curcumin On Proliferation Of Human Oral Squamous Cell Carcinoma Cells And Its Possible Mechanism

ObjectiveCurcumin is a Chinese turmeric active ingredient with antioxidant, anti-tumor, anti-inflammatory, seavenging free radicals, anti-microbial effect, et al. Particularly, the anti-tumor effect of curcumin has attracted a lot of attention by scholars, and many research has been done on the anti-tumor effect and mechanism of Curcumin. It has been confirmed that Curcumin can inhibit many tumor cells proliferation and induce tumor cells apoptosis. However, the study of the anti-tumor effect of Curcumin on the squamous cell carcinoma of the head and neck is rarely reported. In this study, different concentrations of curcumin were used to act on human oral squamous cell carcinoma cells. By investigating the effects of curcumin in inhibiting proliferation and inducing apoptosis in oral squamous cell carcinoma in vitro, we mainly focus on its possible molecular mechanism.MethodsTea8113 and Tb cell lines were commonly cultured, and observed with inverted microscope. Different concentrations of curcumin (6.25,12.50,25.00, and50.00μmol/L) were used to act on Tca8113 and Tb cells for 24 h, MTT were used to evaluate the growth inhibition rate of Tca8113 and Tb. Morphological assay and flow cytometry were employed to detect apoptosis. The expression ofβ-catenin and Notch1 was analyzed by immunocytochemistry.Results1. The morphological changes such as chromatic agglutination, karyopyknosis, and nuclear fragmentation could be seen in part of apoptotic cells after treated with curcumin with inverted microscope.2. The proliferation of Tca8113 and Tb were inhibited significantly by curcumin in a does-dependent manner.3. The apoptosis rate was significantly increased after treated with curcumin.4. The expression ofβ-catenin was significantly down-regulated after treated with curcumin for 24 hours, while the level of Notch1 was up-regulated significantly.Conclusion1. Curcumin could inhibit proliferation and induce apoptosis of oral squamous cell carcinoma Tca8113 and Tb cells.2. The possible molecular mechanism might be related to the modulation ofβ-catcnin and Notchl levels.