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Inhibition of histone deacetylase (HDAC) modu- lates the expression of many genes and induces cell cycle arrest, apoptosis, and differentiation in sev- eral cancer cell lines. Melanoma is a malignant phase of cutaneous melanocytes originally derived fromthe neural crest and is highly metastatic. A ther- apeutic agent capable of inducing differentiation of metastatic melanoma cells into a nonmalignant stage would be useful to prevent metastasis. We exam- ined whether HDAC inhibitors can induce differen- tiation of the murine melanoma cell line B16-BL6 into neural-type cells in vitro. A morphologic change accompanied by extended dendrites was induced in melanoma cells after treatment with the HDAC in- hibitors butyrate and trichostatin A (TSA). The al- tered morphology was similar to that of neural cells. Many of the extended dendrites fused with other dendrites of neighboring cells and had synapse-like knobs on their dendrites. These dendrites showed positive labeling with anti-α/β-tubulin and anti-L1 cell adhesion molecule (L1CAM) antibodies but were seldom stained with phalloidin, suggesting that the neural cell-related proteins were major components of the extended dendrites but that actin stress fibers were not. Furthermore, the mature neuron-specific

journal of health science

Differentiation of B16-BL6 Melanoma Cells into Microtubule-Associated Protein 2-Positive Cells after Treatment with the Histone Deacetylase Inhibitors Butyrate and Trichostatin A