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Antibiotic Tetrocarcin-A Down-regulates JAM-A, IAPs and Induces Apoptosis in Triple-negative Breast Cancer Models

Sri Harikrishna Vellanki1, Rodrigo G B Cruz1, Cathy E Richards1

  • 1Department of Surgery, Royal College of Surgeons in Ireland, Dublin, Ireland.

Anticancer Research
|March 8, 2019
PubMed
Abstract

Insights

Tetrocarcin-A, a compound that down-regulates junctional adhesion molecule-A (JAM-A), effectively reduced triple-negative breast cancer (TNBC) cell viability and tumor growth. This suggests Tetrocarcin-A

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Triple-negative breast cancer (TNBC) presents limited therapeutic options due to the absence of key receptor targets.
  • Elevated junctional adhesion molecule-A (JAM-A) expression correlates with aggressive TNBC phenotypes.

Purpose of the Study:

  • To assess the anti-tumor efficacy of Tetrocarcin-A, a JAM-A-down-regulating compound, in TNBC models.
  • To investigate the molecular mechanisms underlying Tetrocarcin-A's bioactivity in TNBC.

Main Methods:

  • Evaluated TNBC cell viability, colony formation, and xenograft growth following Tetrocarcin-A treatment.
  • Assessed protein expression of cell fate signaling pathways, including apoptosis, via immunoblotting.
  • Compared Tetrocarcin-A effects with transient JAM-A gene silencing.

Main Results:

  • Tetrocarcin-A significantly reduced TNBC cell viability in vitro and in vivo.
  • Tetrocarcin-A induced JAM-A down-regulation, decreased ERK and c-FOS phosphorylation, and inhibited IAP proteins.
  • The compound triggered a caspase-dependent intrinsic apoptotic pathway.

Conclusions:

  • Tetrocarcin-A demonstrates potent anti-cancer activity against TNBC.
  • Tetrocarcin-A's mechanism involves modulating JAM-A, ERK, c-FOS, and apoptotic pathways.
  • Tetrocarcin-A warrants further development as a novel therapeutic agent for TNBC.
Keywords:
Tetrocarcin–ATriple negative breast cancerapoptosischorionic allantoic membrane assayjunctional adhesion molecule-Anatural compounds

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