It is important to note that our results were not the same as those in neural crest cells and HPTCs in which RGC-32 is a downstream target of Smad pathways, indicating that the activation pathway and effect of RGC-32 between normal development and carcinogenesis
may be controlled by different mechanisms. Finally, by means of transwell cell migration assay we further showed that RGC-32 mediated TGF-β-induced cell migration in BxPC-3 cells, implicating that RGC-32 helps to enhance metastatic phenotype in vitro. Conclusions To sum up, an important issue addressed in this study is that RGC-32 might be a novel metastasis promoting factor for pancreatic cancer and it enhances metastatic phenotype by mediating TGF-β-induced EMT independent of Smad pathway in pancreatic cancer cell line BxPC-3. #NCT-501 datasheet randurls[1|1|,|CHEM1|]# These findings described for the first time the role of RGC-32 in the progression of pancreatic cancer
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