Preclinical Evaluation of Discorhabdins in Antiangiogenic and Antitumor Models

Mar Drugs. 2018 Jul 19;16(7):241. doi: 10.3390/md16070241.

Abstract

Elements of the hypoxia inducible factor (HIF) transcriptional system, a key regulator of the cellular hypoxic response, are up-regulated in a range of cancer cells. HIF is fundamentally involved in tumor angiogenesis, invasion, and energy metabolism. Inhibition of the transcriptional activity of HIF may be of therapeutic benefit to cancer patients. We recently described the identification of two marine pyrroloiminoquinone alkaloids with potent activity in inhibiting the interaction between the oncogenic transcription factor HIF-1α and the coactivator protein p300. Herein, we present further characterization data for these two screening hits: discorhabdin H (1) and discorhabdin L (2), with a specific focus on their anti-angiogenic and anti-tumor effects. We demonstrated that only discorhabdin L (2) possesses excellent anti-angiogenic activity in inhibiting endothelial cell proliferation and tube formation, as well as decreasing microvessel outgrowth in the ex vivo rat aortic ring assay. We further showed that discorhabdin L (2) significantly inhibits in vivo prostate tumor growth in a LNCaP xenograft model. In conclusion, our findings suggest that discorhabdin L (2) represents a promising HIF-1α inhibitor worthy of further drug development.

Keywords: HIF; alkaloids; angiogenesis; discorhabdins; hypoxia; marine natural products.

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Animals
  • Antineoplastic Agents / pharmacokinetics*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Drug Evaluation, Preclinical
  • E1A-Associated p300 Protein / metabolism
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Gene Expression Regulation, Neoplastic / drug effects
  • Heterocyclic Compounds, 4 or More Rings / pharmacology*
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Male
  • Mice
  • Mice, SCID
  • Neovascularization, Pathologic / drug therapy*
  • Neovascularization, Pathologic / metabolism
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / metabolism
  • Quinones / pharmacology*
  • Rats
  • Signal Transduction / drug effects

Substances

  • Angiogenesis Inhibitors
  • Antineoplastic Agents
  • Heterocyclic Compounds, 4 or More Rings
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Quinones
  • discorhabdin H
  • discorhabdin L
  • E1A-Associated p300 Protein