This indicates that CCL18 might use several receptors and the balance of the receptor expression might regulate the agonistic and antagonistic effects of CCL18. In AbMole Succinylsulfathiazole conclusion, our data demonstrate that CCL18 induces EMT in A549 cells, enhances their metastatic potential and supports chemotherapy resistance. Thus, CCL18 is not only a mediator released by tumor-associated macrophages and potentially reflecting the tumor size but it also influences neoplastic processes of adenocarcinoma. The data presented here demonstrate that CCL18 is able to trigger events involved in tumor metastasis such as change from primary epithelial tumor cells into migratory mesenchymal cells, chemotaxis, and invasion. In addition, CCL18 also protects tumor cells from chemotherapy by increasing chemoresistance. Thus, we conclude that CCL18 will be a future target in the treatment of lung cancer. The unconventional, non-muscle, class V myosins play an important role in the transport of intracellular vesicles along actin filaments to membrane docking sites. The isoform myosin Va has been shown to be crucial in the trafficking of melanosomes in melanocytes and in the secretion of granules in neuroendocrine cells. Mutations in the Myo5a gene lead to Griscelli syndrome type 1 in humans, a rare inherited autosomal recessive disorder characterised by hypopigmentation and neurological impairment. In mice, myosin Va mutations result in the dilute phenotype with a lighter coat colour and lethal neurological defects. A variety of proteins involved in the regulation of granule transport has been described to interact with myosin Va. In melanocytes, the cargo-carrying C-terminal tail of myosin Va binds to the exophilin melanophilin which in turn interacts with Rab27, a GTP-binding protein of the Ras superfamily. Knockout of Rab27a/b in mice and Griscelli syndrome type 2 in humans, caused by mutation of the Rab27a gene, both show platelet defects resulting in increased bleeding times and a reduction in the number of dense granules, indicating that Rab27 is a key player in platelet dense granule biogenesis and secretion. The secretion of intracellular granules from platelets is essential in the process of thrombosis. Upon activation, platelets release a wide array of mediators from their dense and a-granules. Dense granules contain pro-aggregating factors, which sustain and enhance initial platelet responses. In addition to molecules involved in thrombus formation, a-granules also store a range of proteins and receptors involved in other patho-physiological processes, such as inflammation. As Rab27 is known to be associated with myosin Va cargo vesicles and myosin Va is highly expressed in both human and mouse platelets, it is of great interest to determine the role of this motor protein in platelet granule secretion and formation. This could reflect the small size of the platelet, and its extensive plasma membraneassociated target membrane system, the open canalicular system. This is comprised of multiple invaginations of the membrane, forming target sites for fusion of exocytotic vesicles throughout the cell. Effectively, this may mean that the majority of secretory vesicles may already be in a primed and docked position, and that there is no need for myosin-dependent trafficking. It might however be assumed that vesicles require trafficking to platelets within the megakaryocyte, and therefore that myosins may be required for this step.