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The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells

Zhangle Zhou1, Rune Thomsen, Søren Kahns

  • 1Department of Human Genetics, Aarhus University, Denmark.

Biochemical and Biophysical Research Communications
|July 6, 2010
PubMed

Insights

The NSD3L histone methyltransferase acts as a tumor suppressor in breast cancer. Its depletion promotes cell cycle progression and increases cancer cell invasiveness, suggesting a role in restraining metastatic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Aberrations in the NSD3 (WHSC1L1) histone methyltransferase gene are linked to various cancers, including leukemia, lung, and breast carcinomas.
  • This suggests a potential role for NSD3 in the process of carcinogenesis.

Purpose of the Study:

  • To investigate the function of the NSD3L isoform, which possesses the catalytic SET-domain, in human breast cancer cells.
  • To identify genes regulated by NSD3L and elucidate its role in cellular signaling pathways relevant to cancer.

Main Methods:

  • Utilized siRNA-mediated depletion of NSD3L in human breast cancer cells.
  • Performed genome-wide microarray analysis to identify NSD3L-regulated genes.
  • Assessed cell cycle progression and cellular invasiveness following NSD3L depletion.

Main Results:

  • Identified NSD3L-regulated genes involved in cell growth, cell cycle, cell motility, transcription, and apoptosis.
  • Observed up-regulation of cell cycle regulators E2F2 and Arl2 upon NSD3L depletion.
  • NSD3L depletion led to increased cell populations in S and G2/M phases and enhanced invasiveness of MDA-MB-231 cells.

Conclusions:

  • NSD3L plays a significant role in regulating cell cycle progression and restraining cellular metastatic potential.
  • The presented data strongly suggest that NSD3L functions as a tumor suppressor in breast cancer.

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