The Mechanism Of Interaction Between P53 And Septin 2 After UV Irradiation

The tumor suppressor gene p53 is a transcription factor which mediates several cellular processes including growth arrest,apoptosis,differentiation, and DNA damage repair. In the absence or inactivation of p53, the cell cycle can not be stagnant and unable to prepare for apoptosis, so the cells appear cancerous. Mutation in the tumor suppressor gene p53 has been turned out to be the most common genomic variation in human cancer.Wild-type p53 gene play an important role in the control of cell cycle and induction of apoptosis. Introducting exogenous wild-type p53 gene or p53 protein into tumor cell is a potent therapeutic strategy for human cancer. The present paper reviews the characteristic, research progress and mechanism of tumor suppressor gene p53 in human cancer.The septins are a family of proteins which are broadly distributed in almost all of eukaryotes except plants. Septin was first identified in yeast as a protein that played a role in cytokinesis. Recently, some septin family members participate in the pathogenesis of different diseases including neoplasia, neurodegeneration and infections. These make the research of septins a hallmark in cell biology and pathology.In our research, we observed p53 affect the level of phosphorylation of septin 2 after UV radiation through the stress pathway. The stability of septin2,6,7 complex is enhancive as septin 2 phosphorylation increased, thus increasing the stability of actin filaments, making cytokinesis division successfully. We're interested in finding that septin 2 phosphorylation level changing can influence p53 ser15 phosphorylation site after UV irradiation, and then to inhibit p53 protein activity and reduce its stability. This reaction between p53 and septin2 is important to the regulation of cytokinesis through changing activity and stability of p53.Taken together, it is one of the mechanisms for septin 2 being regulated by p53 and involving in the process of cytokinesis. Through the research work, we hope to provide some theoretical principle to intensively explain the process between the signaling pathways of p53 downstream and the function of septin 2 protein.