Furthermore, we deeply mined the integrated large-scale datasets from public microarrays and immunohistochemistry to validate the overexpression of BIRC5 and SQSTM1 while down-regulated FOXO1 expression in HCC.
Additionally, plasmid-based siRNA against Birc5 and/or Hspa5 were constructed and transfected into the human hepatocellular liver carcinoma cell line, HepG2.
Compared the same and different activated and inhibited BIRC5 network with GO analysis between no-tumor hepatitis/cirrhosis and HCC, our result showed BIRC5 cell cycle network weaker transcription factor activity in both no-tumor hepatitis/cirrhosis and HCC (1); stronger nucleus protein binding but weaker cytoplasm protein binding in no-tumor hepatitis/cirrhosis (2); stronger cytoplasm protein phosphatase binding but weaker ubiquitin-protein ligase activity in HCC (3).
Targeting of X-linked inhibitor of apoptosis protein or survivin by short interfering RNAs sensitize hepatoma cells to TNF-related apoptosis-inducing ligand- and chemotherapeutic agent-induced cell death.
[Effect of inhibiting survivin expression with antisense oligodeoxynucleotides on sensitivity of hepatocellular carcinoma cell lines HepG2 and HepG2/ADM to adriamycin].
[Effect of inhibiting survivin expression with antisense oligodeoxynucleotides on sensitivity of hepatocellular carcinoma cell lines HepG2 and HepG2/ADM to adriamycin].