AURKB and intrahepatic cholangiocarcinoma: The results showed that down-regulated inhibition and overexpression of AURKB boosted the proliferation, cell cycle, invasion, migration and metastasis of ICC in vivo and in vitro. To better explore the latent mechanism of AURKB promoting ICC progression, we conducted a sequence of experiments to testify that AURKB discrepant expression can affect the tumorigenicity and proliferation of ICC cells, as well as influence EMT.