β-Catenin Expression Regulates Cell Migration of Human Colonic Adenocarcinoma Cells Through Gelsolin.

Background/aim: β-Catenin is one of the key players in colonic carcinogenesis. Being part of the E-cadherin complex, it regulates cell-cell adhesion and the migratory ability of cells. However, the role of nuclear β-catenin in the cell migration process is poorly understood.

Gelsolin interacts with LamR, hnRNP U, nestin, Arp3 and β-tubulin in human melanoma cells as revealed by immunoprecipitation and mass spectrometry.

Gelsolin, a multifunctional actin binding protein, plays a not yet fully understood role in tumorigenesis. Therefore the goal of this study was to identify additional molecular partners of gelsolin in human melanoma cells, separately in the cytoplasmic compartment and cell nuclei. For this purpose we performed immunoprecipitation experiments based on a modified protocol followed by mass spectrometry.

Active invadopodia of mesenchymally migrating cancer cells contain both β and γ cytoplasmic actin isoforms.

Invadopodia are actin-rich protrusions formed by mesenchymally migrating cancer cells. They are mainly composed of actin, actin-associated proteins, integrins and proteins of signaling machineries. These protrusions display focalized proteolytic activity towards the extracellular matrix.

β- and γ-Actins in the nucleus of human melanoma A375 cells.

Actin is a highly conserved protein that is expressed in all eukaryotic cells and has essential functions in the cytoplasm and the nucleus. Nuclear actin is involved in transcription by all three RNA polymerases, chromatin remodelling, RNA processing, intranuclear transport, nuclear export and in maintenance of the nuclear architecture. The nuclear actin level and polymerization state are important factors regulating nuclear processes such as transcription.

Analysis of gelsolin expression pattern in developing chicken embryo reveals high GSN expression level in tissues of neural crest origin.

Gelsolin is one of the most intensively studied actin-binding proteins. However, in the literature comprehensive studies of GSN expression during development have not been performed yet in all model organisms. In zebrafish, gelsolin is a dorsalizing factor that modulates bone morphogenetic proteins signaling pathways, whereas knockout of the gelsolin coding gene, GSN is not lethal in murine model.