Generally, carcinomas which originate in epithelial cells and sarcomas which originate in mesenchymal cells (e.g., osteosarcoma) are thought to be quite different in their tumorigenesis as well as in the phenotypes including cytoskeleton, binding molecules, proliferation procedure, and surface glycoproteins [9, 10]. Therefore, different therapeutic approaches have been employed for the treatment of sarcomas, if compared with the therapies applied for

the treatment of carcinomas, except for the Entinostat surgical treatment. On the other hand, the existence of cell surface-bound sugar chain structures, which are common among carcinomas and sarcomas, Inhibitors,research,lifescience,medical but not present in normal cells, has been suggested [11]. Moreover, the concept of epithelial-mesenchymal transition in tumors implies common structures and/or mechanism among carcinomas and sarcomas [12, 13]. Therefore, on the basis of our previous in vitro and in vivo studies with ESA bound to Span 80 vesicles for targeting carcinoma cells [6], we found it worthwhile to investigate Inhibitors,research,lifescience,medical whether the lectin ESA can also be applied in a therapeutic Inhibitors,research,lifescience,medical approach against osteosarcomas. Span 80 is generally known in the

food and cosmetic industries as sorbitan monooleate, although commercial Span 80 is a heterogeneous mixture of sorbitan mono-, di-, tri-, and tetra-esters [14]. We have already demonstrated that nonionic vesicles prepared from Span 80 have promising Inhibitors,research,lifescience,medical physicochemical properties (high membrane fluidity with temperature dependent fusiogenicity) which make this type of vesicle an attractive possible alternative to the commonly used liposomes in vitro and in vivo [6, 14–22]. Aim of the work was to clarify the specificity of the binding of ESA to either OST cells or LM8 cells, both being osteosarcoma cell lines. Furthermore, the potential Inhibitors,research,lifescience,medical effectivity of ESA as ligand on the surface of Span 80 vesicles [6, 14, 18, 19,

21, 22] with targeting function and as possible apoptosis-inducer for the treatment of osteosarcoma was also examined. In however the work presented, the interactions between ESA and OST cells and between ESA and LM8 cells were examined by means of fluorescence microscopy and flow cytometry. As a result of our study, the evidence is presented that ESA specifically binds to these two types of osteosarcoma cells, followed by induction of apoptosis due to this specific ESA binding to the cells. Furthermore, we could demonstrate that ESA has a considerable potential as novel type of ligand immobilized onto PEGylated Span 80 vesicles, an important step towards the potential development of a therapy for the treatment of refractory osteosarcoma, as novel lipidic microcapsule drug-delivery system (DDS) for transporting and delivering anticancer drugs for the treatment of cancer [6]. 2. Material and Methods 2.1.

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