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Updated: Dec 26, 2025

Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
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The histone demethylase KDM2B activates FAK and PI3K that control tumor cell motility

Nefeli Zacharopoulou1,2, Galatea Kallergi1, Saad Alkahtani1,3

  • 1Department of Biochemistry, University of Crete Medical School, Voutes, Greece.

Cancer Biology & Therapy
|March 17, 2020
PubMed

Insights

The histone demethylase KDM2B regulates tumor cell motility by activating Focal Adhesion Kinase (FAK) and phosphoinositide-3 kinase (PI3K) signaling pathways. This finding reveals a novel role for KDM2B in prostate cancer cell migration.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • KDM2B is a histone demethylase previously shown to regulate epithelial markers, small GTPases, and the actin cytoskeleton in cancer cells.
  • The role of KDM2B in regulating tumor cell motility, particularly through signaling pathways like Focal Adhesion Kinase (FAK), remains largely unexplored.

Purpose of the Study:

  • To investigate the role of KDM2B in the activation of FAK signaling.
  • To determine KDM2B's involvement in regulating tumor cell motility.
  • To elucidate the specific signaling pathways modulated by KDM2B in prostate and colon cancer cells.

Main Methods:

  • Quantitative Reverse Transcription PCR (RT-PCR) for gene expression analysis.
  • Western blotting to assess protein expression and activity.
  • Wound-healing assays to evaluate cell migration.
  • Pharmacological inhibition using a phosphoinositide-3 kinase (PI3K) inhibitor (LY294002).

Main Results:

  • KDM2B overexpression or silencing modulated FAK activity in DU-145 prostate and HCT-116 colon tumor cells, independent of FAK gene transcription or protein levels.
  • KDM2B overexpression significantly enhanced migration in DU-145 cells, an effect abrogated by PI3K inhibition, indicating FAK/PI3K pathway involvement.
  • Knockdown of KDM2B downregulated the p85-PI3K subunit, while overexpression led to its upregulation in DU-145 cells.

Conclusions:

  • KDM2B plays a novel role in regulating FAK/PI3K signaling activation in prostate cancer cells.
  • KDM2B's modulation of the FAK/PI3K pathway is critical for controlling prostate cancer cell motility.
  • These findings highlight KDM2B as a potential therapeutic target for managing prostate cancer progression.
Keywords:
FAKKDM2BPI3Kmigrationprostate cancer

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