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Proteomic investigation of anti‐tumor activities exerted by sinularin against A 2058 melanoma cells
Author(s) -
Su TzuRong,
Lin JenJie,
Chiu ChienChih,
Chen Jeff YiFu,
Su JuiHsin,
Cheng ZhiJiao,
Hwang WenIng,
Huang Han Hsiang,
Wu YuJen
Publication year - 2012
Publication title -
electrophoresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.666
H-Index - 158
eISSN - 1522-2683
pISSN - 0173-0835
DOI - 10.1002/elps.201100462
Subject(s) - melanoma , apoptosis , annexin , flow cytometry , western blot , cell cycle , microbiology and biotechnology , cancer research , downregulation and upregulation , chemistry , cell growth , cell , heat shock protein , biology , biochemistry , gene
The extracts from soft corals have been increasingly investigated for biomedical and therapeutic purposes. The aim of this study is to examine and analyze the anti‐tumor effects of the genus S inularia extract sinularin on A 2058 melanoma cells using MTT assay, cell migration assay, wound healing assay, flow cytometric analysis, and proteomic analysis. Sinularin dose‐dependently (1–5 μg/mL) inhibited melanoma cell proliferation while the treatment at identical concentrations suppressed cell migration. Sinularin dose‐dependently enhanced apoptotic melanoma cells and caused tumor cell accumulation at G 2/ M phase, indicating that sinularin exerts apoptosis‐induced and cell cycle‐delayed activities in A 2058 melanoma cells. Comparative proteomic analysis was conducted to investigate the effects of sinularin at the molecular level by comparison between the protein profiling of melanoma cells treated with sinularin and without the treatment. Thirty‐five differential proteins (13 upregulated and 22 downregulated) concerning the treatment were identified by liquid chromatography‐tandem mass spectrometry. Proteomic data and W estern blot displayed the levels of several tumor inhibitory or apoptosis‐associated proteins including annexin A 1, voltage‐dependent anion‐selective channel protein 1 and prohibitin (upregulated), heat shock protein 60, heat shock protein beta‐1, and peroxiredoxin‐2 (downregulated) in A 2058 melanoma cells exposed to sinularin. Increased expression of p53, cleaved‐caspase‐3, cleaved‐caspase‐8, cleaved‐caspase‐9, p21, and B ax and decreased expression of B cl‐2 in sinularin‐treated melanoma cells suggest that the anti‐tumor activities of sinularin against melanoma cells are particularly correlated with these pro‐apoptotic factors. These data provide important information for the mechanisms of anti‐tumor effects of sinularin on melanoma cells and may be helpful for drug development and progression monitoring of human melanoma.