Results of a study on the effect of Notch signaling pathway inhibitors on ameloblastoma cell invasion

Abstract

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 AfÏliated 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 AfÏliated 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.