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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2006-1-6
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pubmed:abstractText |
The human gene Hugl-1 (Llgl/Lgl1) has significant homology to the Drosophila tumor suppressor gene lethal(2)giant larvae (lgl). The lgl gene codes for a cortical cytoskeleton protein, Lgl, that is involved in maintaining cell polarity and epithelial integrity. We speculate that Hugl-1 might play a role in epithelial-mesenchymal transition (EMT) and that loss of Hugl-1 expression plays a role in the development or progression of malignant melanoma. Thus, we evaluated melanoma cell lines and tissue samples of malignant melanoma for loss of Hugl-1 transcription. We found that Hugl-1 was downregulated or lost in all cell lines and in most of the tumor samples analysed, and that these losses were associated with advanced stage of the disease. Reduced Hugl-1 expression occurred as early as in primary tumors detected by both immunohistochemical and reverse transcription-polymerase chain reaction (RT-PCR) analysis. Functional assays with stable Hugl-1-transfected cell lines revealed that Hugl-1 expression increased cell adhesion and decreased cell migration. Further, downregulation of MMP2 and MMP14 (MT1-MMP) and re-expression of E-cadherin was found in the Hugl-1-expressing cell clones supporting a role of Hugl-1 in EMT. Our studies thus indicate that loss of Hugl-1 expression contributes to melanoma progression.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cadherins,
http://linkedlifedata.com/resource/pubmed/chemical/Cytoskeletal Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/LLGL1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/MMP14 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 14,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinases,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinases...,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
5
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
103-10
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16170365-Blotting, Western,
pubmed-meshheading:16170365-Cadherins,
pubmed-meshheading:16170365-Cell Adhesion,
pubmed-meshheading:16170365-Cell Line, Tumor,
pubmed-meshheading:16170365-Cell Movement,
pubmed-meshheading:16170365-Cytoskeletal Proteins,
pubmed-meshheading:16170365-Disease Progression,
pubmed-meshheading:16170365-Down-Regulation,
pubmed-meshheading:16170365-Epithelium,
pubmed-meshheading:16170365-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16170365-Humans,
pubmed-meshheading:16170365-Immunohistochemistry,
pubmed-meshheading:16170365-Matrix Metalloproteinase 14,
pubmed-meshheading:16170365-Matrix Metalloproteinase 2,
pubmed-meshheading:16170365-Matrix Metalloproteinases,
pubmed-meshheading:16170365-Matrix Metalloproteinases, Membrane-Associated,
pubmed-meshheading:16170365-Melanoma,
pubmed-meshheading:16170365-Microscopy, Fluorescence,
pubmed-meshheading:16170365-Neoplasm Invasiveness,
pubmed-meshheading:16170365-Proteins,
pubmed-meshheading:16170365-RNA,
pubmed-meshheading:16170365-RNA, Messenger,
pubmed-meshheading:16170365-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16170365-Tissue Distribution,
pubmed-meshheading:16170365-Transcription, Genetic,
pubmed-meshheading:16170365-Transfection
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pubmed:year |
2006
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pubmed:articleTitle |
Expression of Hugl-1 is strongly reduced in malignant melanoma.
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pubmed:affiliation |
Institute of Pathology, University Regensburg, Regensburg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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