p53可诱导细胞周期阻滞、凋亡、分化、静息、DNA损伤、血管生成和转移抑制。最新研究表明,p53作为转录因子,通过作用于α(Ⅱ)胶原脯氨酰-4-羟化酶(α2PH)、Ras、调控损伤的自噬调节剂(DRAM)和糖酵解与凋亡的p53诱导型调节剂(TIGAR)的基因分布,抑制肿瘤细胞血管生成和肿瘤细胞运动,促进细胞自我吞噬作用的发生和诱导糖酵解与凋亡。p53也可作为蛋白质分子直接与鼠双微体2(MDM2)发挥相互作用,在细胞质中锚定至线粒体从而诱导肿瘤细胞凋亡。p53新的作用及作用机制的阐明有助于为癌症治疗提供理论依据和开发更多有效的抗肿瘤药物。
Tumor suppressor p53 is known as the ‘ guardian of the genome' owing to its most important functions on tumor growth in vivo and vitro. It has been reported that p53 can induce cell cycle arrest, DNA damage,angiogenesis, and metastasis inhibition. The newest developments of p53 show that as a transcription factor, p53 triggers alpha ( Ⅱ ) PH, Ras, DRAM, glycolysis and TIGAR to induce inhibition of angiogenesis, motility, improve autophagy and irduce glycolysis and apoptosis. As a protein,p53 itself binds to MDM2 and then regulates apoptosis. The elucidation of p53 mechanism is helpful for cancer therapy.