Discover Oncology (Jun 2023)

AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression

  • Peng Ma,
  • Ying Hao,
  • Wei Wang,
  • Yue-Feng Zhang,
  • Kai-Huan Yu,
  • Wei-Xing Wang

DOI
https://doi.org/10.1007/s12672-023-00707-1
Journal volume & issue
Vol. 14, no. 1
pp. 1 – 12

Abstract

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Abstract Intrahepatic cholangiocarcinoma (ICC) is a fatal disease and the molecular mechanism of its progression remains unknown. Aurora Kinase B (AURKB) is a central regulator of chromosome separation and cytokinesis and is abnormally expressed in a variety of cancer cells. This research aimed to explore the effect of AURKB in occurrence and metastasis of ICC. We found that AURKB showed a progressive up-regulation pattern from normal bile duct tissue to ICC with high invasion. Our data showed that AURKB significantly promoted ICC cell proliferation, induced epithelial-mesenchymal transition (EMT), migration and invasion through gain- and loss- of function experiments. In vivo results consistently showed that AURKB up-regulation not only promoted tumor growth, but also promoted tumor metastasis. Importantly, we discovered that AURKB regulates the expressions of EMT-related genes via PI3K/AKT signaling axis. Herein, our results suggest that AURKB induced EMT through the activation of PI3K/AKT signaling pathway is critical to the progression of ICC, which may be a prospective therapeutic treatment for overcoming ICC metastasis and progression.