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Hic‐5 affects proliferation, migration and invasion of B16 murine melanoma cells
Author(s) -
Noguchi Fumihito,
Inui Shigeki,
Nakajima Takeshi,
Itami Satoshi
Publication year - 2012
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/pcmr.12005
Subject(s) - rhoa , melanoma , gene silencing , focal adhesion , biology , cancer research , small hairpin rna , motility , coactivator , microbiology and biotechnology , signal transducing adaptor protein , cell migration , cell growth , context (archaeology) , phenotype , regulator , rna interference , metastasis , signal transduction , cell , cancer , cell culture , rna , gene knockdown , genetics , transcription factor , gene , paleontology
Summary Hic‐5 is a shuttling protein between the cell membrane and the nucleus which functions as a focal adhesion adaptor protein and a nuclear receptor coactivator. Although several studies have shown its involvement in other types of cancer, the role of Hic‐5 in melanoma is unknown. Herein, we show for the first time that Hic‐5 is expressed in B16‐F1 murine melanoma cells. To determine its function in melanoma cells, we used shRNA‐mediated RNA interference and established stable clones with down‐regulated Hic‐5 expression. These clones had impaired growth and metastatic potential compared with controls in vivo, which correlated with decreased proliferation, migration and invasion in vitro. Moreover, silencing of Hic‐5 expression in B16‐F1 activated RhoA with an amoeboid phenotypic change, indicating that Hic‐5 is a key regulator of B16‐F1 metastasis in the context of Rho‐dependent motility. These results provide new evidence that Hic‐5 is a possible molecular target for treatment of melanoma.