However, a vast number of the studies revealed quite diverse functionality of CCN2, which obviously represents the property of this molecule as a CCN family member, as summarized in Table 1. Therefore, it is not surprising that nearly 10 different names have been assigned to this single molecule during the progression of research on CCN2 [1], [3], [4] and [5]. Most critical

biomolecules possess a dark side as well as a bright side of their functions. In this point of Selleckchem BMS387032 view, CCN2 is a typical double-edged sword in various microenvironments. Indeed, CCN2 is involved in physiological events during the development and growth of a variety of organ and tissues [1] and [10], particularly of mesenchymal http://www.selleckchem.com/products/NVP-AUY922.html ones. Positive aspects of the functional properties of CCN2 are also represented by the potential of

this molecule to accelerate the regeneration of damaged tissues, including bone and cartilage [12] and [13]. Of note, even a cardioprotective effect of CCN2 against myocardial ischemia-reperfusion injury was reported [14]. Most relevant reports describe the positive effects of CCN2 on cell growth and differentiation [9] and [10], save for one showing the dedifferentiation of skeletal muscle cells induced by CCN2 [15]. Contrarily, it is also widely recognized that CCN2 is a major mediator of fibrotic disorders and a critical determinant of the phenotype of certain malignancies. Involvement of CCN2 in fibrosis of multiple organs was described

in a number of reports [4], [7] and [16], conferring the title of profibrotic molecule on CCN2. As listed in [75] and [76], pathogenic involvement of the CCN2 gene is frequently observed in a large number of types of malignant tumors, including cancers that originate in the epidermis [4], [7], [10] and [17]. These findings may indicate the possible contribution of CCN2 to epidermal-mesenchymal transition (EMT) events, because this factor acts as a key player Dolichyl-phosphate-mannose-protein mannosyltransferase in mesenchymal tissue development. However, the role of CCN2 in determining the malignant phenotype is still controversial and complicated. It has been solidly indicated that CCN2 promotes bone metastasis of breast cancers [5] and [10], whereas its overexpression rather shifts the phenotype of oral cancer cells toward a benign one [18] and [19]. How can CCN2 action have such apparently opposite outcomes? As briefly stated in the previous section, the multiple biological outcomes effected by CCN2 are conferred by multiple interactions with a vast number of collaborative molecules (Fig. 1). In fact, CCN2 is reported to interact with multiple molecular counterparts from different categories [7], [10], [20], [21], [22] and [23], which are summarized in Table 2. This interaction with a variety of collaborators enables CCN2 to execute apparently contradictory missions, i.e.