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Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
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Sulforaphane-induced apoptosis involves p53 and p38 in melanoma cells

K Rudolf1, M Cervinka, E Rudolf

  • 1Department of Medical Biology and Genetics, Faculty of Medicine in Hradec Králové, Charles University in Prague, Šimkova 870, 500 38, Hradec Králové, Czech Republic.

Apoptosis : an International Journal on Programmed Cell Death
|December 31, 2013
PubMed

Insights

Sulforaphane (SF) shows anti-cancer effects in melanoma by inducing cell death. While effective in cell lines, its efficiency is lower in fresh melanoma, suggesting potential combination therapies for better outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Malignant melanoma exhibits complex reprogramming of cell death and survival pathways, leading to chemoresistance and poor prognosis.
  • Sulforaphane (SF), a compound from cruciferous plants, has demonstrated antiproliferative and proapoptotic activity in various cancer cell lines, including melanoma.

Purpose of the Study:

  • To investigate the cytotoxic and apoptotic effects of Sulforaphane (SF) on melanoma cell lines and fresh melanoma cultivates.
  • To elucidate the signaling pathways modulated by SF in melanoma, including oxidative stress, DNA damage response, and apoptosis-related proteins.

Main Methods:

  • Treatment of melanoma cell lines and fresh melanoma cultivates with Sulforaphane (SF).
  • Assessment of cytotoxicity and apoptosis induction (mitochondrial, caspase-dependent).
  • Analysis of signaling pathways, including oxidative stress markers, DNA-damage response, p38 kinase activity, Akt activity, and expression of proapoptotic proteins (Bax, Puma).

Main Results:

  • SF demonstrated cytotoxicity and induced mitochondrial, caspase-dependent apoptosis in melanoma cell lines, with lower efficiency in fresh cultivates.
  • SF triggered oxidative stress, DNA-damage response, altered p38 kinase activity, and increased Bax and Puma expression in melanoma cells.
  • In p53-mutant cells, Puma expression was p38-dependent; in fresh cultivates, Akt-mediated suppression of p38 and p53 potentially reduced SF-induced apoptosis.

Conclusions:

  • SF inhibits growth and induces mitochondrial apoptosis in both melanoma cell lines and fresh cultivates.
  • The proapoptotic effects of SF may be enhanced by combining it with Akt inhibitors, particularly in patient-derived melanoma samples.
  • SF warrants further preclinical investigation as a single agent or in combination therapies for melanoma treatment.

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