p16、cyclin D1在消化道癌细胞周期调控中的关系探讨

P16和cyclinD1是参与细胞周期调控及维持细胞正常增殖的关键蛋白,通过G1/S监测点即R点（restriction point）发挥调控作用。cyclinD1与CDK4/6（细胞周期依赖性激酶）结合形成cyclinD1/CDK4/6复合物,促使CDK4/6活化,细胞越过G1/S监测点进入细胞分裂周期。P16可重复地和特异性地与cyclinD1竞争调控CDK4/6,抑制两者的激酶活性,使细胞不能快速通过G1/S转换。由此可见,两者相辅相成、相互制约,其适时适度的表达是细胞周期得以正常运转的前提。近年来,大量的研究结果显示,P16基因的缺失及cyclinD1过度表达与恶性肿瘤发生、发展、及恶化关系密切。因此,对P16和cyclinD1的深入研究将有助于胃肠道肿瘤的分期、疗效判断、预后、转移、复发和治疗。

p16 and cyclin D1 s effect in the cell cycle of digestive tract cancer cell

P16 and cyclinD1 are involved in cell cycle regulation and maintenance of normal cell proliferation of the key protein. They play a regulatory role in the restriction point, cyclinD1 combined with CDK4 / 6 cyclinD1 / CDK4 / 6 complexes start the CDK4 / 6 and the cells to enter the cell division cycle. P16 can be repeated and specific competition with cyclinD1 control CDK4 / 6, inhibiting the kinase activity of both, so that cells can not be fast through the GI / S conversion. It can be seen that the two complement each other, mu- tual restraint, and its expression in a timely manner appropriate to the cell cycle is a prerequisite for normal operation. In recent years, a large number of studies have shown, P16 gene deletion and cyclinDl malignant over-expression and the occurrence and development of, and deterioration of close ties. Therefore, P16 and cyclinDl-depth study will contribute to the staging of gastrointestinal tumors, determine the efficacy, prognosis, metastasis and recurrence and treatment.