The Study On Interactions Between S100A2/S100A6 And Wnt/β-Catenin Signalling Pathway

BACKGROUNDS AND OBJECTIVES:The development and progession of tumor is a complex biologic process that involves various factors and numerous genes. Tumor cells are characterized of deregulated proliferation, attributed to the abnormality of signalling pathways. Wnt/β-catenin pathway is one of these signalling pathways. In this pathway,β-catenin, axin, adenomatous polyposis coli (APC), glycogen synthase kinase -3β(GSK-3β), and dishevelled (DVL) are the major components which regulate the degradation ofβ-catenin. Secreted Wnt ligands act on the cell surface receptor Frizzled and activate DVL. Activated DVL inhibits the phosphorylation ofβ-catenin by GSK-3β, and then blocksβ-catenin degradation so thatβ-catenin accumulates and translocates to the nucleus, where it interacts with the T cell factor 4 (TCF4) transcription factor and induces the transcription of target genes such as c-jun, c-myc, and cyclin D1. Defects in the components of the Wnt/β-catenin signalling pathway, upregulateβ-catenin / TCF4 activity, therefore promote tumorigenesis and tumour progression. Upregulatedβ-catenin / TCF4 activity is a pivotal event in most human tumors.