中文摘要：

背景与目的：作为ING1的一种主要表达产物，p33^ING1b蛋白结合和稳定p53后诱导肿瘤细胞周期阻断或引起细胞凋亡。本研究通过建立高表达p33^ING1b的鼻咽癌细胞HNE1模型，探讨p33^ING1b对鼻咽癌细胞增殖影响及分子作用机制。方法：利用脂质体介导转染HNE1细胞，RT—PCR法筛选p33^ING1b高表达的阳性克隆，绘制生长曲线检测细胞增殖速度，免疫组化法检测细胞中p53的表达分布，流式细胞术检测细胞周期，Western blot法检测p53、p21、Stat3、C-myc和Cyclin D1蛋白水平。结果：转染ING1后p33^ING1b表达水平显著升高，HNE1细胞增殖能力受到抑制，出现G0／G1期的阻滞、S期比例下降。细胞中Stat3、C—myc和CyclinD1表达水平显著降低，p53与p21表达水平上升。结论：p33^ING1b可能通过促进HNE1细胞中p53和阻断Stat3两种不同信号传导通路抑制鼻咽癌细胞的增殖。

英文摘要：

Background and purpose： As a candidate tumor suppressor gene, p33^ING1b can induce cell cycle arrest or cell apoptosis by binding and stabilizing with p53. This study was to evaluate the role of p33^ING1b in the regulation of proliferation of nasopharyngeal carcinoma. Methods： ING1 was transfected into nasopharyngeal carcinoma cell lines HEN1 by lipofectamine, then, the clone with p33^ING1b overexpression was selected with RT-PCR. The rate of cell proliferation was determined by cell growth curve. Distribution of p53 was examined by immunohistochemistry. Cell cycle was measured by flow cytometry. Protein expression of p53, p21, Stat3, C-myc and CyclinD1 were examined by Western blot. Results： p33^ING1b overexpression can markedly inhibit cell growth of HNE1. 65% of the cells were arrested at the G0/G1 stage. p33^ING1b could induce p53 accumulation in nucleus and up-regulate expression of p53 and p21, expression of Stat3, C-myc and CyclinD1 were strongly inhibited. Conclusions： p33^ING1b may perhaps inhibit HNE1 cell growth through p53 and Stat3 signal transduction pathway independently.