To study the mechanisms involved in the increase of tumor malignization, different assays comparing the gene expression of non-invasive and pro-invasive tumors after the antiangiogenic treatment were developed. These analyses generated a list of candidate genes that could be responsible for the invasive process, with CD44 among them. In this thesis, we have studied the role of CD44 in the tumor invasion and migration processes using in vitro and in vivo models of renal carcinoma. We have explored the signaling pathway that could be induced due to the CD44 activation. The Src signaling route was possibly shown to be involved in the invasive process of cancer cells. The mechanism responsible for CD44 activation has also been investigated. Between different candidates, Serglycin appeared as a possible ligand and inducer of CD44. Thus, this thesis opens different study ways to determine the molecules responsible for tumor invasion after antiangiogenic treatment and develop new different strategies to overcome the resistance.
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