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NDY1/KDM2B functions as a master regulator of polycomb complexes and controls self-renewal of breast cancer stem

Filippos Kottakis1, Parthena Foltopoulou1, Ioannis Sanidas1

  • 1Authors' Affiliation: Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts.

Cancer Research
|May 24, 2014
PubMed

Insights

The histone demethylase NDY1/KDM2B promotes cancer growth and stem cell self-renewal. Inhibiting NDY1 halts tumor growth by affecting cell cycle progression and differentiation, offering a potential therapeutic target.

Area of Science:

  • Epigenetics and Cancer Biology
  • Stem Cell Biology
  • Gene Regulation

Background:

  • The JmjC domain histone demethylase NDY1/KDM2B is frequently overexpressed in diverse human cancers.
  • NDY1/KDM2B plays a role in regulating gene expression through histone modification.

Purpose of the Study:

  • To investigate the role of NDY1/KDM2B in cancer cell proliferation, self-renewal, and differentiation.
  • To elucidate the molecular mechanisms by which NDY1/KDM2B influences cancer stem cell properties.

Main Methods:

  • Knockdown of NDY1 in various human cancer cell lines.
  • Assessment of anchorage-dependent and independent growth, senescence, apoptosis, and cell cycle progression.
  • Analysis of mammosphere formation and stem cell marker expression (ALDH, CD44, CD24).
  • Orthotopic injection of modified tumor cells in animal models.
  • Investigation of miRNA regulation and polycomb complex targeting.
  • Correlation analysis of NDY1/KDM2B, miRNA, and polycomb target expression in human breast cancer tissues.

Main Results:

  • NDY1 knockdown inhibited cancer cell growth, induced senescence/apoptosis, and blocked G1 progression across multiple tumor types.
  • NDY1 inhibition reduced mammosphere formation and altered stem cell marker expression, suggesting impaired cancer stem cell self-renewal.
  • NDY1 knockdown led to miRNA de-repression, targeting polycomb complexes (PRC1/PRC2), and promoted tumor cell differentiation.
  • Overexpression of NDY1/KDM2B in triple-negative breast cancer correlated with relapse rates, and its expression inversely correlated with NDY1-regulated miRNAs in primary tumors.

Conclusions:

  • NDY1/KDM2B is essential for cancer stem cell self-renewal and tumor growth.
  • NDY1 acts as a master regulator of miRNAs targeting polycomb complexes, influencing cancer cell plasticity.
  • Targeting NDY1/KDM2B represents a potential therapeutic strategy for cancers, particularly triple-negative breast cancer.

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