作者: SA Ciafrè , G Barillari , L Bongiorno-Borbone , F Wannenes , M Izquierdo
关键词: Angiogenesis 、 Blood vessel 、 Biology 、 In vivo 、 In vitro 、 Tumor progression 、 Viral vector 、 Cancer research 、 Endothelial stem cell 、 Immunology 、 Genetic enhancement
摘要: Angiogenesis, the formation of new blood vessels out pre-existing capillaries, is essential for tumor progression. Many factors have been identified that are able to inhibit angiogenesis. Here, we report construction a tricistronic retroviral vector encoding two inhibitors angiogenesis expressed in mammals: N-terminal fragment rat prolactin (16KrPRL) and secreted form human platelet factor 4 (sPF4). When transduced by this vector, glioblastoma cell line loses its ability promoting endothelial locomotion, initial step angiogenesis, an tube network. In spite encouraging vitro result, however, anti-angiogenic cannot block progression animal models. These results suggest therapeutic strategies aiming through inhibition tumor-associated should not only provide large numbers inhibitors, but also target angiogenic produced cells. Moreover, data described herein may confirm recent findings from other groups which indicate order successfully counteract progression, drugs inhibiting vessel be employed combination with traditional anti-tumor strategies, such as chemotherapy or radiotherapy.