부산대학교 도서관

Introduction: Traditional Chinese medicine has few side effects, and can be used to treat specific diseases. Past studies have found that Shikonin has a therapeutic effect on cancer, but there is still insufficient research on the effect of Shikonin on oral cancer. Once oral cancer turns into a malignant tumor, it will seriously threaten the lives of patients. This study therefore seeks to explore application value of Shikonin treatment on oral cancer cells. Methods: The shikonin and human oral cancer cell lines (SCC-4 ＆ SAS) were used in this study. The intensity of CCK-8 reagent is proportional to the number of viable cells, allowing direct analysis of cell growth and toxicity. Additionally, The In Situ Cell Apoptosis Detection Kit was used to detect cell apoptosis in tumor samples based on the principle of terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL). In animal experiment, a 200 μl cell suspension was then subcutaneously injected into the lower abdomen of each rat. Drug administration began when the tumor reached 100 mm3, and each rat's tumor size and body weight were observed until day 28. All experimental data are presented as mean ± standard error of the mean (mean ± S.E.M). Pairwise comparisons were performed using Student's t-test, and p ＜ 0.05 was considered statistically significant. Results: Our results found that Shikonin can specifically target oral cancer cells and present a doses dependent to inhibit cell growth. Using non-lethal doses to observe the migration and wound healing ability of Shikonin on cancer cells, we also found that Shikonin can effectively inhibit cells through decrease Matrix metalloproteinases levels, which in turn inhibits the ability of cancer cells to migrate and promote wound healing, while reduce the oncogene, such as VEGF-A and VEGF-G released in the early stage of cancer cell angiogenesis and lymphangiogenesis. Meanwhile, as the dose intensifies, it induces cell autophagy and activates the expression of ATG-5, LC-3B, Beclin-1 and related autophagy proteins. Once reaching a lethal dose, it further causes a decrease in the mitochondrial phantom potential and release of calcium ions to induce cell apoptosis. Conclusion: The above results show that Shikonin can induce autophagy and activate the apoptosis pathway of oral cancer cells. In the mouse model, Shikonin was also observed to significantly inhibit the growth of oral cancer and cause apoptosis. A review of the research results found that Shikonin can effectively inhibit the growth and metastasis of oral cancer cells and reduce the related proteins of cancer progression, and because oral cancer is easier to administer to the affected area, it is of great value in clinical development in the future, and it is hoped that it can improve patients' healing and improving the cure rate.