Anti-cancer effect of HS-345, a new tropomyosin-related kinase A inhibitor, on human pancreatic cancer

Cancer Lett. 2013 Sep 28;338(2):271-81. doi: 10.1016/j.canlet.2013.04.002. Epub 2013 Apr 13.

Abstract

Tropomyosin-related kinase A (TrkA) is emerging as an important player in carcinogenic progression. TrkA overexpression, which is associated with cell growth, proliferation, survival, and invasion, has been observed in pancreatic cancer. We therefore synthesized HS-345, a novel TrkA inhibitor, and evaluated its anti-cancer effect and underlying mechanism of action in pancreatic cancer. In this study, HS-345 effectively inhibited the growth and proliferation in three pancreatic cancer cell lines (PANC-1, MIA PaCa-2, and BxPC-3). Activation of the TrkA/Akt signal cascade was also inhibited by HS-345 treatment in a dose-dependent manner. The pro-apoptotic effect of HS-345 was evidenced by increased levels of cleaved caspase-3 and cleaved PARP, and decrease of Bcl/Bax expression via mitochondria membrane potential, as well as elevated numbers of TUNEL-positive apoptotic cells. HS-345 was additionally found to exert anti-angiogenic effect by decreasing the expression of HIF-1α and VEGF, major factors of angiogenesis, which were also demonstrated by the suppression of tube formation and migration of VEGF-treated human umbilical vein endothelial cells along with inhibition of blood vessel formation by HS-345 in a Matrigel plug assay with mice. Results of our investigation show that HS-345 inhibited the TrkA/Akt signaling pathway resulting in cell growth/angiogenesis inhibition and apoptosis induction. Based on our data, we suggest that HS-345 is a potential candidate for treating pancreatic cancer.

Keywords: Angiogenesis; Apoptosis; HS-345; Pancreatic cancer; Tropomyosin-related kinase A (TrkA).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cell Growth Processes / drug effects
  • Cell Line, Tumor
  • Drug Screening Assays, Antitumor
  • Human Umbilical Vein Endothelial Cells / cytology
  • Human Umbilical Vein Endothelial Cells / drug effects
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Neovascularization, Pathologic / drug therapy
  • Pancreatic Neoplasms / blood supply
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology
  • Protein Kinase Inhibitors / pharmacology*
  • Pyridines / pharmacology*
  • Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • Signal Transduction / drug effects
  • Sulfonamides / pharmacology*

Substances

  • Protein Kinase Inhibitors
  • Pyridines
  • Sulfonamides
  • Receptor Protein-Tyrosine Kinases