باثولوجيا الفم

SUMMARY Oral squamous cell carcinoma is one of the main causes of death all over the world. Regarding World Health Organization (WHO) data, cancer is the second most common cause of death after cardiovascular diseases. Although the available curative clinical managements for oral squamous cell carcinoma, including surgical interventions, radiotherapy, and chemotherapy, only 50 – 60 % of patients have a 5–year survival rate. This study was performed to assess the effect of Licochalcone A on cell viability, cell proliferation and apoptosis compared to Paclitaxel in cultured OSCC cell line (SCC-15) as well as to determine the role of Licochalcone A in enhancing the anti-proliferative and apoptosis inducing effects of Paclitaxel. The cultured squamous cell carcinoma cell line (SCC-15) was obtained and divided into three treatment groups: Licochalcone A treated group, Paclitaxel treated group, combined drugs treatment group (Licochalcone A + Pacliatxel) and untreated control group. For cell viability assessment, (SRB) assay was done by testing all treatment groups for 24, 48 and 72 hours after drug exposure in different concentrations. Regarding the immunofluorescent interpretation, Annexin V-FITC Apoptosis Staining / Detection Kit was obtained from Abcam company and was used to assess apoptosis in each treatment group. The fluorescent intensity was visualized under confocal fluorescent microscope. For immunohistochemical examination, IPO-38 mouse monoclonal antibody proliferation marker purchased from Abcam company was used and the stained sections were examined under the light microscope. Mean value for area percent of proliferation marker IPO-38 immunohistochemical staining in the three treatment groups was measured by image analyzer computer system. Our findings revealed that cell viability in Licochalcone A and Paclitaxel treatment groups was decreased in a concentration and time dependent manner compared to the control group. Additionally, the cell viability in combination treatment group showed more and obvious reduction in a concentration and time dependent manner. Moreover, by comparison between all treatment groups over the longest time and highest concentrations, the least cell viability was seen in the combination group. For immunohistochemical findings, comparing the studied groups by ANOVA test and according to the highest concentration for each treatment group among the longest duration (72 hours), the untreated control group of SCC-15 cells showed the highest area percent for IPO-38 immunoexpression while the area percent for IPO-38 decreased in the Licochalcone A group. The Paclitaxel and combination groups of SCC-15 cells showed the lowest area percent of IPO-38 immunoexpression. The P value was statistically highly significant for all compared groups. Regarding the fluorescence microscopic findings and according to the ANOVA test, after 24, 48 and 72 hours at the highest concentrations, Annexin V immunofluorescence levels showed the highest values in the combination group followed by Paclitaxel group then LCA group, while the control group showed the least levels. The difference between the treatment modalities at each time was highly statistically significant. According to our study, we concluded that the addition of Licochalcone A enhanced the effect of Paclitaxel on reducing cell proliferation and inducing apoptosis confirming the concept of having a synergistic effect during cancer treatment. This could be applied to reduce the well-known side effects of Paclitaxel on the cancer patients to improve their quality of life.