Furthermore, there are several

Furthermore, there are several http://www.selleckchem.com/products/BI6727-Volasertib.html recent reports implicating microtubules and the microtubule-organizing center in directing cell polarization and migration (40-42). Our data suggest that MxA may be important in this process, representing a member of a new class of microtubule-associated proteins that regul
Epithelial cell adhesion molecule (Ep-CAM)is a type I transmembrane glycoprotein of Mr 40000Da, expressed in most normal epithelial tissues on the basolateral surface. While no expression is seen on squamous epithelia and hepatocytes, it is detected on colon, gastric, prostatic and lung epithelium (Moldenhauer et al, 1987). Epithelial cell adhesion molecule is thought to function as a homotypic intercellular adhesion molecule (Litvinov et al, 1994).

Its role in epithelial cell adhesion is dynamic and interconnected with E-cadherin (Litvinov et al, 1997). By upregulation of Ep-CAM, E-cadherin-mediated cell adhesion diminishes and the Ep-CAM mediated adhesion becomes predominant. During organogenesis in mice, Ep-CAM exhibits features of a morpho-regulatory molecule, which, for instance, is involved in the development of human pancreatic islets (Cirulli et al, 1998). Epithelial cell adhesion molecule was discovered as one of the first tumour-associated antigens by immunising mice with human colon cancer cells followed by analysis of tumour-specific monoclonal antibodies (Herlyn et al, 1979; Sears et al, 1982). Epithelial cell adhesion molecule was then found to be expressed at a high level and frequency not only on colon cancer tissues but on most human adenocarcinomas (Went et al, 2004) as well as on squamous cell carcinomas (Quak et al, 1990).

In the case of breast and ovarian cancers, Ep-CAM mRNA was found to be more than 100-fold overexpressed relative to normal epithelial tissues (Kim et al, 2003; Osta et al, 2004). Overexpression of Ep-CAM is linked to differentiation and cell proliferation (Jordinson et al, 1999), although the molecular mechanism is still poorly understood. In vitro, its overexpression has been shown to be directly linked to stimulation of the cell cycle and proliferation by upregulating c-myc and cyclin A/E (Munz et al, 2004). In breast cancer cells, inhibition of Ep-CAM expression by small inhibitory RNA diminishes cell proliferation, migration and invasiveness of cells (Osta et al, 2004).

Epithelial cell adhesion molecule gene expression appears to be negatively regulated by TNF-alpha through activation of NF-kappaB (Gires et al, 2001). Upon cell cycle arrest by various chemotherapeutics, Ep-CAM surface expression is enhanced (Flieger et al, 2001; Thurmond et al, 2003). As Ep-CAM is involved in adhesion, differentiation and cell proliferation, an influence of Ep-CAM Carfilzomib expression on survival of cancer patients can be expected.

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