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细胞周期蛋白依赖性激酶抑制剂相关基因的突变和表达失调可直接或间接影响细胞的周期、增殖以及凋亡等功能,与肿瘤的发生发展密切相关。p16能够抑制CDK4/CDK6介导的Rb蛋白产物的磷酸化,其CpG岛异常甲基化参与宫颈癌的发生发展;p21作为p53的下游调节因子,与肿瘤血管的生成、淋巴转移及预后相关;p27作用机制复杂,与乳腺癌预后关系密切,并可恢复耐药乳腺癌细胞对他莫昔芬的敏感性;p57在细胞周期G1到S期的转变中至关重要,其表达程度与部分肿瘤的恶性程度相关,它还参与了肿瘤细胞的凋亡过程。了解这些基因的结构和作用机制,探究其在肿瘤发生、发展中所产生的作用,进而寻找有效治疗靶点,已成为肿瘤分子生物学关注的热点。
Mutations and expression disorders of cyclin-dependent kinase inhibitor-related genes may directly or indirectly affect cell cycle, proliferation and apoptosis, which are closely related to tumorigenesis and development. p16 can inhibit the phosphorylation of CDK4 / CDK6-mediated Rb protein product, and aberrant CpG island methylation is involved in the development of cervical cancer. p21, as a downstream regulator of p53, is associated with tumor angiogenesis, lymph node metastasis and prognosis. The mechanism of p27 is complex and closely related to the prognosis of breast cancer, and can restore the sensitivity of resistant breast cancer cells to tamoxifen; p57 in the cell cycle G1 to S transition is crucial, the extent of its expression and some tumors It is also involved in the apoptotic process of tumor cells. Understanding the structure and mechanism of these genes and exploring their roles in tumorigenesis and development, and then looking for effective therapeutic targets, have become the focus of cancer molecular biology.