中文摘要：

背景与目的：作为黏附蛋白catenin家族中的一员，Delta-catenin蛋白可以促进肿瘤细胞的增殖和侵袭，然而其提高肿瘤细胞增殖能力的机制并不清楚。本研究检测了Delta-catenin对肺癌细胞凋亡的影响及其与丝裂原活化蛋白激酶（mitogen-activated protein hinase，MAPK）信号通路蛋白的关系，并初步探索了Delta-catenin促进肿瘤细胞侵袭增殖的可能机制。方法：采用蛋白[质]印迹法（western blot）检测肺癌细胞过表达Delta-catenin前后p38、c-jun氨基末端激酶（c-jun N-terminal kinase，JNK）蛋白活性的变化，同时利用流式细胞术检测了肿瘤细胞凋亡数量的改变，还通过Matrigel基质胶侵袭实验检测了肿瘤细胞侵袭数量的变化。结果：与未处理组和空载体对照组相比，过表达Delta-catenin后肺癌细胞的p38蛋白活性没有变化（P〉0．05），但JNK的蛋白活性却显著减少（P〈0．05），与此同时，肿瘤细胞的凋亡比例显著下降（P〈0．05），而肿瘤细胞的侵袭能力却明显增强（P〈0．05）。结论：Delta-catenin可能通过抑制肺癌细胞JNK通路的活性而减少肿瘤细胞的凋亡，进而促进肿瘤细胞的侵袭。

英文摘要：

Background and purpose： As a member of the catenin family, Delta-catenin protein could promote proliferation and invasion of tumor cells, but the accurate mechanism of Delta-catenin promoting cell proliferation is not clear. In the present study, we iUustrated that Delta-catenin＇s effect on cell apoptosis and their relationship with mitogen-activated protein kinase （MAPK） signaling pathway, and the possible mechanism was also explored for Delta- catenin promoting invasion and proliferation of tumor cells. Methods： The alterations of p38 and c-jun N-terminal rinasel JNK protein activity were detected in SPC and SK lung cancer cell lines with Delta-catenin overexpression or not, by Western blot method. At the same time, the apoptotic number of tumor cells was also examined by FCM method. Furthermore, the number of invasive tumor cells was examined by Matrigel invasive experiment. Results： Compared with untreated group and empty vector group, the activity of p38 protein was unchanged in lung cancer cell lines with Delta-catenin overexpressed （P〉0.05）, but the activity of JNK protein was decreased significantly （P〈0.05）, meanwhile, apoptotic proportion of tumor cells were also reduced （P〈0.05）, and invasive ability of tumor cells was enhanced significantly （P〈0.05）. Conclusion： Delta-catenin probably decreases apoptosis number of lung cancer cells via inhibiting the activity of JNK pathway, and then promotes invasive ability of tumor cells.