Among the transcription factors we examined, the expression of slug was increased by the down-regulation of GEP100, which was unexpected. Slug is a member of the Snail superfamily and first identified as a development protein critical for neural crest formation in chick embryos. Slug is inversely correlated with BU 4061T molecular weight E-cadherin expression and is a critical EMT-promoting factor in many tumor types. Recent study showed that Slug expression was not always associated with E-cadherin down-regulation. It was clearly shown that Slug expression was increased in pancreatic cancer compared with the surrounding parenchyma. However, in the 36 cases of ductal adenocarcinoma analyzed, no obvious relation was found between E-cadherin and Slug expression. In this study we found that GEP100 down-regulation induced an increased E-cadherin expression as well as increased Slug expression. One interpretation is that the E-cadherin protein expression is not dependent on Slug in this cell type and indeed the mRNA of E-cadherin was not changed. Although the expression of Slug is associated with many tumor prognosis, It is not clear yet how Slug itself is regulated. Our data indicated that GEP100 might be involved in the regulation of Slug expression. A proper localization of E-cadherin is also critical for its proper function. Cell-surface E-cadherin in epithelial cells is partially internalized and recycled back to the plasma membrane by multiple mechanisms including clathrin-dependent, caveolae-dependent, lipid-raft mediated pathways or macropinocytosis. In epithelial junctions, the dynamics of E-cadherin was also intimately regulated by the ARF proteins. Arf6 GTPase is crucial for E-cadherin endocytosis and recycling. It has been shown that expression of an inactive Arf6T27N protein blocks HGF-induced internalization of E-cadherin, whereas expression of a constitutive active form of Arf6Q67L causes disassembly of adherens junctions. In HepG2 cells, its accumulation at the plasmam membrane. With immunofluorescence study, we found that GEP100 knockdown increased the accumulation of E-cadherin to adherens junctions. We speculate that GEP100 up-regulated the expression of E-cadherin through inhibiting its endocytosis and the following degradation. Further investigation will be necessary to clarify this issue. In summary, our results presented experimental evidence that GEP100 expression correlated with the invasive ability of pancreatic cancer cells and could be considered as a new target for developing therapeutics to prevent pancreatic cancer cell invasion. Strong evidence indicates that treatment of hypertension not only reduces the risk of cardiovascular diseases, but also delays the progression of CKD. Recently, it has been demonstrated that even having prehypertension or the earliest stages of CKD is associated with an increased risk of cardiovascular diseases. Thus, adequate blood pressure control appears to be critical for the prevention of cardiovascular diseases and progression of CKD. However, to what extent blood pressure should be controlled is still controversial.