we found TIP-1 as one driving force of tumor onset， initial and infiltration. Biochemical analyses with microarrays and antibody arrays suggested that TIP-1 might utilize multiple pathways， such as modulating fibronectin gene expression and uPA protein secretion， to establish or maintain a pro-angiogenic tumor microenvironment. Molecular studies identify β-PIX as a TIP-1 interacting protein. Knockdown of TIP-1 resulted in aberrant localization of β-PIX and activation of Rho GTPase， further regulated the tumor cells migration and invasion. In this study， we also found TIP-1 confered resistance of glioma cells to IR through binded with LZAP to enhance p53 ubiquitination. In vivo studies indicated that depleting TIP-1 inhibited tumor regrowth after IR treatment in a mouse xenograft model. Taken together， this study provided the first ever evidences showing that TIP-1 represents one novel prognostic biomarker and one novel approach to rescue the p53 functionality for an improved radiotherapy of malignant gliomas. The primary challenge in malignant glioma treatment is the lack of prognostic and therapeutic biomarker for the infiltrative growth of tumor cells. We here report TIP-1 protein is over-expressed in high grade gliomas and is associated with glioma tissue/cell morphological changes and poor prognosis of glioma patients. By using orthotopic and heterotopic mouse models of human glioblastomas
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