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NCL1, a highly selective lysine-specific demethylase 1 inhibitor, suppresses prostate cancer without adverse effect

Toshiki Etani1, Takayoshi Suzuki2, Taku Naiki1

  • 1Department of Nephro-Urology, Nagoya City University, Graduate School of Medical Sciences, Nagoya, Japan.

Oncotarget
|January 22, 2015
PubMed

Insights

A novel histone lysine demethylase 1 (LSD1) inhibitor, NCL1, effectively reduced prostate cancer cell viability and tumor growth. This potential therapeutic agent demonstrated efficacy in hormone-resistant prostate cancer without adverse events.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Prostate cancer, particularly hormone-resistant forms, remains a significant clinical challenge.
  • Histone lysine demethylase 1 (LSD1) is frequently overexpressed in prostate cancer, suggesting its role in cancer progression.

Purpose of the Study:

  • To investigate the therapeutic potential of a novel LSD1 inhibitor, NCL1, in prostate cancer models.
  • To evaluate the effects of NCL1 on prostate cancer cell viability, gene expression, cell cycle, and apoptosis.

Main Methods:

  • Treatment of hormone-sensitive (LNCaP) and castration-resistant (PC3, PCai1) prostate cancer cells with NCL1.
  • Assessment of LSD1 expression, cell viability, H3K9me2 accumulation via ChIP, cell cycle distribution, apoptosis, and autophagy markers (LC3-II).
  • In vivo efficacy study in mice bearing PCai1 tumors.

Main Results:

  • NCL1 significantly decreased prostate cancer cell viability and suppressed tumor growth in mice.
  • NCL1 induced H3K9me2 accumulation, G1 cell cycle arrest, and apoptosis.
  • NCL1 treatment led to the induction of autophagosomes and autolysosomes, with increased LC3-II expression.

Conclusions:

  • NCL1 demonstrates significant therapeutic potential as an LSD1 inhibitor for prostate cancer, including hormone-resistant types.
  • NCL1 effectively suppressed prostate cancer growth with no observed adverse effects in preclinical models.
  • Elevated LSD1 expression in human prostate cancer specimens supports its role as a therapeutic target.

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