Abstract:
:Expression of the p75 neurotrophin receptor (p75(NTR)) in primary melanomas is associated with deeply invasive lesions. In turn, there is expression of high levels of neurotrophins at the invasion front of normal tissue adjacent to brain metastases, thus implicating this growth factor-receptor system in melanoma tumorigenesis. The neurotrophins nerve growth factor (NGF) and neurotrophin-3 (NT-3) are potent chemotactic agents for human melanoma cells which express p75(NTR)in vitro. Here we show that the actin-bundling protein fascin specifically interacts with p75(NTR) in an NGF-dependent manner by co-immunoprecipitation and colocalization in melanoma cells that express the two proteins endogenously. In addition, expression of a fascin point mutant at the serine phosphorylation site (serine 39) regulating actin binding abrogates neurotrophin-induced migration. These results suggest a causal role for NGF-mediated dephosphorylation of serine 39 on fascin in mediating actin binding and subsequent melanoma cell migration.
journal_name
Oncogenejournal_title
Oncogeneauthors
Shonukan O,Bagayogo I,McCrea P,Chao M,Hempstead Bdoi
10.1038/sj.onc.1206561subject
Has Abstractpub_date
2003-06-05 00:00:00pages
3616-23issue
23eissn
0950-9232issn
1476-5594pii
1206561journal_volume
22pub_type
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