Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-7-31
pubmed:abstractText
As with most cancers, the aetiology of human cutaneous melanoma is likely to be multifactorial and to include the accumulation of irreversible alterations in an unknown number of genes. Elucidating this molecular progression necessitates both the identification of genetic perturbations at each clinically relevant stage, and the assessment of their impact on the normal melanocyte. The observation that the epidermal melanocyte, in contrast to metastatic melanoma cells, requires activation of the protein kinase C (PKC) pathway to facilitate growth in vitro indicates that one or more isoforms (or substrates) of this large and complex family of proteins are among those that undergo alteration during the development of malignant melanoma. Consequently, a number of studies have investigated the expression of various PKC family members in both melanocyte and melanoma cell lines, without a consensus of opinion as to which isoforms are of biological significance in melanoma development and progression. The present study involved a comprehensive evaluation of the PKC profile in normal melanocytes and in 16 metastatic melanoma cell lines. The results show that the major difference in isoform expression between epidermal melanocytes and melanoma cells is the loss of PKCbeta protein expression in 90% of melanoma cell lines. Examination of PKCbeta in benign and malignant melanocytic lesions revealed that this protein is either downregulated or absent in both naevi and metastatic melanomas. We conjecture that, although the loss of PKCbeta expression is a common phenomenon in malignant melanocytes, it may be related more to a normal process of melanocytic differentiation than to malignant transformation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0960-8931
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
355-69
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11479424-Blotting, Western, pubmed-meshheading:11479424-Cell Differentiation, pubmed-meshheading:11479424-Cell Extracts, pubmed-meshheading:11479424-Cell Line, pubmed-meshheading:11479424-Cell Membrane, pubmed-meshheading:11479424-Cell Size, pubmed-meshheading:11479424-Cell Transformation, Neoplastic, pubmed-meshheading:11479424-Cytosol, pubmed-meshheading:11479424-Down-Regulation, pubmed-meshheading:11479424-Gene Expression Profiling, pubmed-meshheading:11479424-Gene Expression Regulation, Enzymologic, pubmed-meshheading:11479424-Gene Expression Regulation, Neoplastic, pubmed-meshheading:11479424-Humans, pubmed-meshheading:11479424-Immunohistochemistry, pubmed-meshheading:11479424-Isoenzymes, pubmed-meshheading:11479424-Melanocytes, pubmed-meshheading:11479424-Melanoma, pubmed-meshheading:11479424-Neoplasm Invasiveness, pubmed-meshheading:11479424-Protein Kinase C, pubmed-meshheading:11479424-Protein Transport, pubmed-meshheading:11479424-RNA, Messenger, pubmed-meshheading:11479424-RNA, Neoplasm, pubmed-meshheading:11479424-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11479424-Tumor Cells, Cultured
pubmed:year
2001
pubmed:articleTitle
Loss of expression of protein kinase C beta is a common phenomenon in human malignant melanoma: a result of transformation or differentiation?
pubmed:affiliation
American Health Foundation, Valhalla, NY 10595, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.