Background: There are many theories to explain the origin and development of cancer, and it is a multistep process. It depends on many genes that control functions such as growth, proliferation, migration, invasion, metastasis, and angiogenesis. Ameloblastoma is a tumor of odontogenic epithelium, 80% of which occur in the jaw and often painlessly enlarge the jaw and cause facial deformity. Although ameloblastoma is a benign tumor, it is a locally invasive tumor and has a recurrence rate of up to 90% after surgery. It can also transform into cancer. According to the results of the researchers, ameloblastoma cells grow and infiltrate. The current standard treatment for ameloblastoma includes osteotomy, which is divided into marginal mandibular, segmental maxillary, partial maxillary, or total maxillary resection, depending on the location of the tumor. Although these surgical treatments are somewhat effective, the results often result in jaw deformity and facial deformity. Therefore, it is necessary to actively search for specific therapeutic strategies. Recent studies have begun to investigate the relationship between the activation of abnormal signaling pathways and ameloblastoma invasion. The complex interactions between signaling pathway elements, target genes, and molecular entities regulate tumor cell growth, apoptosis, and other key pathological phenomena in various signaling pathways. The results of other researchers have shown that the Notch signaling pathway is important in promoting ameloblastoma cell invasion. However, the role of the Notch signaling pathway and its related proteins in ameloblastoma cell invasion remains unclear. Our study investigated how inhibition of the Notch signaling pathway affects ameloblastoma cell invasion and investigated the relationship between them. We conducted a study to determine how this pathway affects ameloblastoma cell invasion by inhibiting the Notch signaling pathway in ameloblastoma cells. Aim: To investigate the effect of Notch signaling pathway inhibitors on ameloblastoma cell invasion. Materials and Methods: The study was conducted at the Experimental Research Base of Affiliated Hospital of Chifeng University, Inner Mongolia, China, using quantitative research methods and experimental research designs. The effect of FLI-06 on the infiltration of AB cells after inhibition of the Notch signaling pathway was studied by Transwell method. The ameloblastoma cell lines used in the study were obtained from the Experimental Research Base of Affiliated Hospital of Chifeng University. The Notch signaling pathway inhibitor FLI-06 was purchased from Absin Bioscience Inc. (Absin® CAS: 313967-18-9), Shanghai. Results: After staining the cells in the Transwell (Lower chamber) with Amethyst dye, the number of AB cells inhibited by FLI-06 was observed under a microscope. The cell permeability of the control group was estimated to be 100%, while the cell permeability of the experimental group was 25%. The infiltration activity of ameloblastoma cells was 1.37±0.06%, and the number of infiltrating cells was 137.20±25.55, while the infiltration activity of normal oral mucosa cells was 0.12±0.01%, and the number of infiltrating cells was 80.40±3.36. The number of AB cells after inhibition with FLI-06 was 34.60±6.95, and the number of cells in the control group using simple culture medium was 137.20±25.55. Conclusion Inhibition of the Notch signaling pathway with FLI-06 reduced ameloblastoma cell invasion

Background: Ameloblastoma (AB) is an odontogenic epithelial tumor. 80% of ameloblastomas occur in the jaw and often painlessly enlarge the jaw and cause facial deformity. Ameloblastoma is usually treated with a complete osteotomy, which is divided into three types: partial maxillary marginal resection, maxillary sinus resection, and total maxillary resection. These surgical procedures cause jaw deformity and facial trauma, so effective treatment methods with minimal trauma are still being sought in medicine. In order to develop new drugs for the treatment of ameloblastoma, it is necessary to study the molecular mechanisms that inhibit the proliferation of cancer cells. In recent years, it has been established that ameloblastoma is caused by abnormal activation of signaling pathways. Multiple signaling pathway regulators, target genes, and molecular interactions are involved in tumor cell proliferation and apoptosis. Previous studies have shown that blocking key signaling pathways is not only a therapeutic option in clinical practice, but also a useful tool in selecting tumor resection sites. Therefore, studying the molecular level of the Notch signaling pathway in the proliferation of ameloblastoma cells is of great importance for the treatment of the disease. Studies have shown that many factors of the Notch signaling pathway play important roles in promoting or inhibiting different tumors. The Notch signaling pathway promotes tumor cell proliferation by regulating CDK1, Cyclin D1, HES-1, and COX-2. Chinese researchers Li Wenchao and Baolidao’s research team have studied factors related to AB proliferation and invasion for the past decade, and have identified the roles of factors such as COX-2, Survivin, Akt, and PI3K in AB proliferation and invasion, and have successfully cultured primary ameloblastoma cells. However, the exact role of the Notch signaling pathway in AB cell proliferation has not been clearly studied. Aim: To study the effect of Notch signaling pathway inhibitors on ameloblastoma cell proliferation. Materials and Methods: The study was conducted at the Experimental Research Base of Affiliated Hospital of Chifeng University, Inner Mongolia, China, using quantitative research methods and experimental research designs. The expression of Notch1, Cyclin D1, and CDK1 genes in AB cells was detected using real-time polymerase chain reaction. The effect of FLI-06 on the proliferation of AB cells after inhibition was studied by counting (CCK8) method. The ameloblastoma cell lines used in the study were obtained from the Experimental Research Base of Affiliated Hospital of Chifeng University. The Notch signaling pathway inhibitor FLI-06 was purchased from Absin Bioscience Inc. (Absin® CAS: 313967-18-9), Shanghai. Results: In the study, real-time polymerase chain reaction analysis showed that the expression of Cyclin D1 in AB cells was 7.01 times higher than that in normal oral mucosa cells, the expression of CDK1 was 2.63 times higher, and the expression of Notch1 was 4.95 times higher. The cell proliferation of the control group was calculated as 100% by the AB cell proliferation inhibitor (CCK8) method, and compared with the experimental group, the cell proliferation of the group added with 5.0μM FLI-06 was 53.98%, 46.53% in the 10.0μM concentration group, and 22.33% in the 20.0μM concentration group. Conclusion Notch1, Cyclin D1, and CDK1 expression in ameloblastoma were significantly different from that in normal oral mucosa cells. Inhibition of the Notch signaling pathway with FLI-06 reduced ameloblastoma cell proliferation.

Abstract: In addition to citing from the old medical scriptures by Indian, Tibetan, and Mongolian medical scholars, “Mthong ba dga’ byad” by Jigmeddanzanjamts, also contains a number of prescriptions of Chinese medicine that were widely used in Chinese medical practice at that time. Therefore, crude drugs and prescriptions of Chinese medicine in this book has a great significance, but there are few studies done in the last decades. Purpose: To make selection of Chinese herbal medicines and recipes from the book “Mthong ba dga’ byad” by Jigmeddanzanjamts and explain them. Research methods: Research methods in ancient textbook, check list, analysis and synthesis methods were used. Conclusion It was clarified that in the book “Mthong ba dga’ byad” by Jigmeddanzanjamts there are 44 names of herbal medicines and prescriptions of Chinese origin, and some prescriptions are explained. According to these herbal medicines and prescriptions, Mongolian doctors and maarambas used not only Indian Ayurvedic and Tibetan medicines, but also Chinese medicines and prescriptions in their medical care.