SC1 limits tube formation, branching, migration, expansion and induce apoptosis of endothelial cells

Sezer Akgol1, Batuhan Mert Kalkan2, Dogacan Yucel3

  • 1Department of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Istanbul, Turkey.

Vascular Pharmacology
|September 5, 2021
PubMed

Insights

Small molecule SC1 inhibits tumor angiogenesis by reducing endothelial cell proliferation and increasing apoptosis. This compound shows promise as an anticancer therapy targeting tumor blood vessel formation.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Endothelial cells (ECs) are crucial for tumor growth, supplying nutrients and promoting angiogenesis.
  • Targeting ECs is a key strategy in cancer therapy to inhibit tumor progression.
  • ERK1/2 signaling in ECs is a potential therapeutic target, with small molecule SC1 showing specific activity.

Purpose of the Study:

  • To investigate the effects of SC1 on endothelial cell proliferation, apoptosis, and angiogenesis.
  • To evaluate SC1's potential as an anticancer agent targeting tumor angiogenesis.

Main Methods:

  • Viability, apoptosis, cell cycle, gene expression, wound closure, and tube formation assays were performed on ECs treated with SC1.
  • Western blot analysis was utilized to examine protein expression and pathway activation.

Main Results:

  • SC1 demonstrated significant antiangiogenic effects, inhibiting EC expansion, tube formation, branching, and migration.
  • SC1 suppressed EC proliferation in a dose-dependent manner.
  • SC1 treatment increased EC apoptosis, upregulating pathways involving BAK1, Stat1, Sox4, and Caspase1.

Conclusions:

  • SC1 exhibits potent antiangiogenic and anti-proliferative effects on endothelial cells.
  • SC1 induces apoptosis in endothelial cells through specific molecular pathways.
  • SC1 is a promising candidate for developing novel anticancer therapies targeting tumor angiogenesis.