桥粒由许多蛋白质组成,包括钙黏着蛋白,Armadillo蛋白质和plakoplilin,负责介导细胞-细胞粘附。钙粘蛋白是跨膜蛋白,在相邻细胞上相互结合,在细胞之间形成牢固的粘合。在正常组织中,桥粒通过将细胞保持在一起有助于维持组织的结构完整性。在致癌过程中,桥粒的结构和功能可能发生改变。例如,在口腔癌中,某些钙粘蛋白的表达可能会增加,导致细胞-细胞粘附增加和更具粘性的肿瘤块。这可能有助于癌细胞逃避免疫系统和抵抗化疗的能力。除了它们在细胞粘附中的作用,桥粒也在细胞信号传导中起作用。构成桥粒的蛋白质可以与调节细胞增殖的信号通路相互作用,迁移和生存。这些途径的失调可能有助于口腔癌的发展和进展。也有证据表明桥粒可能参与了侵袭和转移的过程,即癌细胞从原发肿瘤扩散到身体其他部位。已破坏或异常桥粒的癌细胞可能更有可能迁移并侵入其他组织。总的来说,桥粒似乎在口腔癌的发生和发展中很重要。需要进一步的研究来充分了解这些细胞-细胞连接在疾病中的作用,并确定潜在的治疗靶标。
Desmosomes are composed of a number of proteins, including cadherins, armadillo proteins and plakoplilins, which are responsible for mediating cell-cell adhesion. Cadherins are transmembrane proteins that bind to each other on adjacent cells, forming a strong adhesive bond between the cells. In normal tissues,
desmosomes help to maintain the structural integrity of the tissue by holding the cells together. During carcinogenesis, the structure and function of
desmosomes may be altered. For example, in oral cancer, the expression of certain cadherins may be increased, leading to increased cell-cell adhesion and a more cohesive tumour mass. This may contribute to the ability of cancer cells to evade the immune system and resist chemotherapy. In addition to their role in cell adhesion,
desmosomes also play a role in cell signaling. The proteins that make up desmosomes can interact with signaling pathways that regulate cell proliferation, migration and survival. Dysregulation of these pathways may contribute to the development and progression of oral cancer. There is also evidence that desmosomes may be involved in the process of invasion and metastasis, which is the spread of cancer cells from the primary tumour to other parts of the body. Cancer cells that have disrupted or abnormal desmosomes may be more likely to migrate and invade other tissues. Overall,
desmosomes appear to be important in the development and progression of oral cancer. Further research is needed to fully understand the role of these cell-cell junctions in the disease and to identify potential therapeutic targets.