关键词: Delta-catenin, 肺癌, 细胞凋亡, c-jun氨基末端激酶通路

Abstract: 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 illustrated 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 Deltacatenin 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.

Key words: Delta-catenin, Lung cancer, Cell apoptosis, c-jun N-terminal kinase pathway