Exploring the apoptotic potential of Prunus spinosa Trigno extract in BRAF-mutated melanoma cells

Alessia Di Pauli1,2, Rosa Vona3, Alice Di Netta2

  • 1Department of Anatomy, Histology, Forensic-Medicine and Orthopedics, Section of Histology and Embryology, Sapienza University of Rome, Rome, 00161, Italy.

Abstract

Insights

The novel compound Prunus spinosa Trigno + Nutraceutical Activator Complex (PsT + NAC®) effectively reduced melanoma cell viability and induced cell death. This compound also altered cell migration and triggered apoptosis in BRAF-mutant melanoma cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Melanoma is an aggressive cancer characterized by invasion and metastasis.
  • Developing effective treatments for melanoma remains a critical challenge.

Purpose of the Study:

  • To investigate the anti-melanoma effects of the patented compound Prunus spinosa Trigno + Nutraceutical Activator Complex (PsT + NAC®).
  • To evaluate the impact of PsT + NAC® on primary, metastatic, and malignant human melanoma cell lines.

Main Methods:

  • Cell viability assays were performed on WM115, WM266-4, and A375 melanoma cell lines.
  • Morphological changes, cell migration, cell cycle, and apoptosis were analyzed.
  • Western blotting was used to assess autophagic and apoptotic pathways.

Main Results:

  • PsT + NAC® significantly reduced melanoma cell viability in a dose- and time-dependent manner.
  • Treatment induced morphological changes indicative of irreversible cell death and altered cell migration.
  • Cell cycle arrest (G2/M or G1) and apoptosis (sub-G1 increase) were observed, with higher concentrations triggering caspase-dependent apoptosis.
  • Lower concentrations induced a protective autophagic response.

Conclusions:

  • PsT + NAC® demonstrates significant efficacy in inhibiting the growth of BRAF-mutant melanoma cells.
  • The compound induces cell death through apoptosis and modulates cellular processes like migration and cell cycle progression.