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Haploinsufficient tumor suppressor Tip60 negatively regulates oncogenic Aurora B kinase

Arnab Bose1, Surabhi Sudevan, Vinay J Rao

  • 1Transcription and Disease Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, Karnataka, India.

Journal of Biosciences
|January 3, 2020
PubMed

Insights

Aurora kinase B (AurkB) stability and activity are regulated by acetylation. Tip60, a tumor suppressor, acetylates AurkB, impacting its function and potentially influencing cancer development.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Aurora kinases, particularly Aurora kinase B (AurkB), are critical for mitosis.
  • Dysregulated AurkB expression is linked to malignant phenotypes.
  • Mechanisms regulating AurkB stability and activity outside of mitosis are not well understood.

Purpose of the Study:

  • To investigate the regulation of Aurora kinase B (AurkB) stability and activity.
  • To explore the role of acetylation in AurkB function.
  • To uncover the interplay between AurkB and lysine acetyltransferases (KATs).

Main Methods:

  • In vitro acetylation assays using purified AurkB and KATs (p300 and Tip60).
  • Identification of acetylated lysine residues on AurkB.
  • Assessment of the impact of acetylation on AurkB protein stability and kinase activity.

Main Results:

  • AurkB undergoes in vitro acetylation by p300 and Tip60.
  • Tip60 acetylates two conserved lysine residues in the AurkB kinase domain.
  • Acetylation by Tip60 reduces AurkB protein stability and kinase activity.

Conclusions:

  • Tip60-mediated acetylation of AurkB is a novel regulatory mechanism.
  • Downregulation of Tip60 may lead to increased AurkB activity, contributing to carcinogenesis.
  • This study reveals a functional link between AurkB and Tip60 relevant to cancer development.

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