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FGF‐2 blocks TGF‐β1‐mediated suppression of Bcl‐2 in normal melanocytes
Author(s) -
Von Willebrand Maria,
Köhler Klaus,
Alanko Tuomo,
Laiho Marikki,
Saksela Olli
Publication year - 2005
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2005.00277.x
Subject(s) - transforming growth factor , cancer research , medicine , chemistry , endocrinology , microbiology and biotechnology , biology
Normal melanocytes require growth support provided by the adjacent basement membrane. In contrast, nevus cells and melanoma cells survive in the dermis, and in vitro on a soft collagen gel. Transforming growth factor‐β1 (TGF‐β1) produced by melanocytes themselves induces apoptosis in normal melanocytes cultured on collagen gel, an effect that can be counteracted by fibroblast growth factor‐2 (FGF‐2). The purpose of this study was to investigate the mechanisms by which FGF‐2 counteracts the apoptotic signals from TGF‐β1 in melanocytes cultured on collagen gel. We report that FGF‐2 did not interfere with the signal transduction from the TGF‐β1 receptors to SMAD2/3 proteins. Instead, TGF‐β1 decreased the level of Bcl‐2 in normal melanocytes cultured on collagen gel, and FGF‐2 reversed the TGF‐β1‐mediated reduction in the level of Bcl‐2. In nevus and melanoma cells, TGF‐β1 was unable to induce a decrease in the level of Bcl‐2, and treatment with FGF‐2 did not cause an increase in the level of Bcl‐2 in nevus or melanoma cells. In conclusion, our results suggest that a reduction in the level of the anti‐apoptotic Bcl‐2 is involved in the execution of apoptosis induced by TGF‐β1 in normal melanocytes cultured on collagen gel and that FGF‐2 can prevent TGF‐β1 from causing this reduction.