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Updated: Nov 4, 2025

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Adhesion-growth factor crosstalk regulates AURKB activation and ERK signalling in re-adherent fibroblasts

Siddhi Inchanalkar1, Nagaraj Balasubramanian

  • 1Indian Institute of Science Education and Research, Pashan, Pune 411 008, India.

Journal of Biosciences
|May 28, 2021
PubMed

Insights

Cell adhesion and growth factors differentially regulate Aurora kinases, particularly AURKB. Re-adhesion restores AURKB activation, but serum growth factors block this recovery, impacting Erk activation in fibroblasts.

Area of Science:

  • Cell biology
  • Molecular biology
  • Biochemistry

Background:

  • Aurora kinases play distinct roles in cell cycle regulation.
  • Cell-matrix adhesion and growth factors are key regulators of cell cycle processes.
  • Understanding kinase regulation in response to dynamic cellular environments is crucial.

Purpose of the Study:

  • To investigate the differential regulation of Aurora kinases by cell adhesion dynamics.
  • To elucidate the interplay between cell adhesion, growth factors, and Aurora kinase activity.
  • To define the role of Aurora kinases in controlling Erk activation during cell re-adhesion.

Main Methods:

  • Monitoring Aurora kinase (AURKB) activation upon loss and re-adhesion to cell culture substrates.
  • Assessing the impact of serum growth factors on adhesion-dependent AURKB recovery.
  • Utilizing serum treatment and AZD (an AURKB inhibitor) to study kinase cross-talk.
  • Analyzing Erk activation and membrane ruffling as readouts of cellular signaling.

Main Results:

  • AURKB activation decreases upon loss of cell adhesion and recovers upon re-adhesion in serum-deprived conditions.
  • Serum growth factors, even with short exposure, inhibit the adhesion-dependent recovery of AURKB.
  • AURKB activation negatively correlates with Erk activation during re-adhesion.
  • Inhibiting AURKB in serum-deprived re-adherent cells enhances Erk activation and membrane ruffling.

Conclusions:

  • A novel mechanism of Aurora kinase B (AURKB) regulation by the combined effects of cell adhesion and growth factors is identified.
  • This adhesion-growth factor-dependent regulation of AURKB controls Erk activation in re-adherent fibroblasts.
  • The findings highlight a complex signaling network integrating adhesion and growth factor pathways via AURKB and Erk.

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