目的 探讨抗凋亡基因survivin在细胞转化中的作用机制。方法 利用RT-PCR获得survivin编码区序列，双酶切后，将其定向克隆至原核和真核表达载体；生长曲线观察高表达survivin对细胞增殖的影响；软琼脂集落形成实验观察细胞的接触抑制生长能力；Western Blot检测survivin高表达引起的蛋白质分子改变。结果 通过分子克隆，构建survivin原核和真核表达载体，并可在大肠杆菌和真核细胞中表达。生长曲线表明,转染survivin的293细胞的增殖速度略快于对照细胞，尤其在细胞生长至高密度时；Survivin可以明显提高293细胞的软琼脂集落形成能力；Survivin的高表达可以引起癌基因cyclinD1和c-myc的蛋白表达水平增高。结论 抗凋亡基因survivin具有促进细胞转化的作用，这种作用可能依赖于cyclinD1和c-myc的功能。

Overexpression of human pituitary tumor transforming gene (PTTG) is wildly detected in many tumors, including esophageal cancer. Besides overexpression of PTTG in esophageal squamous cell carcinoma (ESCC) tissues and cells, we detected accumulation of cytoplasmic β-catenin in ESCC. In our study, a putative TCF4-binding element (TBE) was identified in PTTG promoter region. The activity of PTTG promoter containing the TBE was activated by S37Aβ-catenin and inhibited by dominant-negative TCF. Furthermore, the activation by S37Aβ-catenin was mostly abrogated among PTTG promoter region without the TBE or with a mutant one. By using biotin-streptavidin pull-down assay, we also found that the TBE among PTTG promoter bound to TCF-4 protein. Moreover, levels of PTTG mRNA and protein were increased by S37Aβ-catenin. Finally, it is noticeable that we detected a correlation between-catenin localization and PTTG expression in 69 primary ESCC (p<0.01). In brief, our study shows that overexpression of PTTG in ESCC is likely due to the activation of β-catenin/WNT signaling. As a target gene of β-catenin/TCF pathway, PTTG may play an important role in tumorigenesis of human ESCC.

Introduction Breast cancer is the leading cause of cancer death in women worldwide. Elevated expression of c-Myc is a frequent genetic abnormality seen in this malignancy. For a better understanding of its role in maintaining the malignant phenotype, we used RNA interference (RNAi) directed against c-Myc in our study. RNAi provides a new, reliable method to investigate gene function and has the potential for gene therapy. The aim of the study was to examine the anti-tumor effects elicited by a decrease in the protein level of c-Myc by RNAi and its possible mechanism of effects in MCF-7 cells.

AIM: To investigate gene expression pattern of human g-synuclein gene in human esophageal squamous cell carcinoma (ESCC) by using semi-quantitive reverse transcription polymerase chain reaction (RT-PCR), and to study the role of g-synuclein in the development of human ESCC.

AIM: To investigate the putative role of human papillomavirus (HPV) infection in the carcinogenesis of esophageal squamous cell carcinoma in China.