TNF-alpha induced junctional modulation enhances response to radiation in Caco-2 cells

The Adhesion molecules mediated cell-cell and cell matrix interactions are essential for variety of physiological and pathological processes including maintenance of normal tissues integrity as well as tumor development and progression. Cell-cell interaction is initiated by interactions of tight junctional proteins with neighboring cells. Tight junctions govern the paracellular permeability of endothelial and epithelial cells. Aberrations of tight junction formation are an early and key event during vascular spread cancer and inflammation. TNF-alpha plays an important role in the intestinal inflammation by increase of intestinal epithelial tight junction permeability. It has been reported that TNF alpha- modulated intestinal epithelial tight junction barrier is mediated by myosin light-chain kinase protein expression through NFk-B activation. However, the alterations of tight junctional proteins involved in the TNF-alpha-induced increase of intestinal TJ permeability remain unclear. Claudin is essential to the formation and maintenance of tight junction (TJ) and has been identified 24 members so far. Claudin-1, 3, 4, 6, 10 and 16 have been shown altered in various cancers and they may have important roles in cell survival, motility, and invasion of cancer cells. However, the functions of these proteins in tumorigenesis and inflammation are still being elucidated