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Imidazole inhibits B16 melanoma cell migration via degradation of beta‐catenin
Author(s) -
Jeong Yun Mi,
Li Hai Lan,
Kim Su Yeon,
Yun HyeYoung,
Baek Kwang Jin,
Kwon Nyoun Soo,
Kim DongSeok
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.895.4
Subject(s) - mg132 , imidazole , protein kinase b , chemistry , cell migration , hacat , phosphorylation , microbiology and biotechnology , cell , cell culture , cancer research , biochemistry , biology , in vitro , proteasome inhibitor , apoptosis , genetics
We investigated whether imidazole inhibits the migration of B16 murine melanoma cells. First of all, we found that imidazole did not show any cytotoxic effect at less than 100 μM in B16 cells and HaCaT cells (normal human keratinocytes). In addition, imidazole had no influence on B16 cell proliferation at the same concentration range. To explore the effects of imidazole on B16 cell migration, we treated imidazole to B16 cells at various concentrations and measured the migration using Scratch Wound Migration Assay. In 6 h, imidazole significantly inhibited B16 cell migration in a concentration‐dependent manner. It is known that migration involves phosphorylation of two signaling pathways; Akt‐ and GSK3β‐activated protein kinase pathway. In 1 h, Western blotting results showed the inhibition of both Akt‐ and GSK3β pathway in imidazole‐treated B16 cells. Moreover, imidazole also led to the degradation of β‐cateninin via GSK3β pathway. Further results showed that MG132, a proteasomal inhibitor, abrogated cell migration by imidazole in B16 cells. Thus, we demonstrate that imidazole inhibits cell migration in B16 cells by β‐catenin degradation. Moreover, we suggest that imidazole may serve as a chemo‐preventive candidate agent for melanoma therapy.