论文部分内容阅读
Annexin A5 is a Ca2?-dependent phospholipidbinding protein and protein kinase C inhibitory protein. It has a potential role in cellular signal transduction, inflammation, growth and differentiation. In this study, we evaluated the expression of this protein in lung tumor tissues and subsequently established a NCI-H520 cell line that stably expresses the wild-type ANXA5 gene to determine the effects of annexin A5 upregulation on the cell morphology, proliferation and metastasis potential in vitro.The effects of annexin A5 on NCI-H520 cells were tested by crystal violet staining, CCK-8 assay, scratch wound assay, and Transwell assay. The expressions of Akt,PCNA, vimentin, and E-cadherin were examined by Western blot assay. In this study, we demonstrated that annexin A5 is expressed at lower levels in tumor tissues compared with normal tissues. Additionally, the upregulation of this protein may inhibit the proliferation, migration, and invasion abilities of NCI-H520 cells in vitro. The transfected cells were arrested in the G1/S phase of the cell cycle, and the expression levels of Akt, PCNA and Vimentin were downregulated, while E-cadherin was upregulated.
Annexin A5 is a Ca2? -dependent phospholipid binding protein and protein kinase C inhibitory protein. It has a potential role in cellular signal transduction, inflammation, growth and differentiation. In this study, we evaluated the expression of this protein in lung tumor tissues and subsequently established a NCI-H520 cell line that stably expresses the wild-type ANXA5 gene to determine the effects of annexin A5 upregulation on the cell morphology, proliferation and metastasis potential in vitro. The effects of annexin A5 on NCI-H520 cells were tested by crystal The expression of Akt, PCNA, vimentin, and E-cadherin were examined by Western blot assay. In this study, we demonstrate that annexin A5 is expressed at lower levels in tumor tissues compared with normal tissues. The upregulation of this protein may inhibit the proliferation, migration, and invasion abilities of NCI-H520 cells in vitro. The tr ansfected cells were arrested in the G1 / S phase of the cell cycle, and the expression levels of Akt, PCNA and Vimentin were downregulated, while E-cadherin was upregulated.