Survivin overexpression in HCC and liver cirrhosis differentially correlates with p-STAT3 and E-cadherin

摘要: Survivin, a member of the family inhibitor apoptosis proteins, functions as key regulator and cell proliferation. Overexpression survivin has been implicated in several human cancers, including hepatocellular carcinoma (HCC). Although factors have shown vitro to upregulate expression cancer cells, vivo regulators hepato-carcinogenesis are largely unknown. We studied by immunohistochemistry protein relation cyclin D1, phosphorylated signal transducer activator transcription 3 (p-STAT3), beta-catenin, E-cadherin phosphorylated-Akt (p-Akt) 69 cases HCC adjacent liver cirrhosis. Survivin was expressed 63/69 (91.3%) 40/47 (85.1%) localization exclusively nuclear, while intense cytoplasmic low nuclear observed correlated significantly with grade tumors, D1 p-STAT3. Expression cirrhosis downregulation expression. There no significant correlation beta-catenin or p-Akt In conclusion, we showed an association well differentiated HCC, cycle D1. Activation STAT3 loss but not Akt pathways seem be upregulation