基因组与蛋白组学技术微小RNA及其在医学的应用.ppt

These results indicated that overexpression of miR-10b is sufficient to promote both migration and invasion in vitro. 5.1 miR-10b? cell migration and invasion in vitro 5.2 miR-10b ? tumour invasion in vivo 5.3 miR-10b ? distant metastasis in vivo 5.4 how miR-10b expression is regulated? 5. 5 What is a direct and functional target of miR-10b? 5.6 miR-10b expression is elevated in metastatic breast tumours 5.2 miR-10b ? tumour invasion in vivo implanted miR-10b-transduced or mock-infected SUM149 cells into the mammary fat pads of NOD-SCID mice(该品系鼠为非肥胖糖尿病/严重联合免疫缺陷鼠，不但成熟T、B细胞联合免疫缺陷，而且单核巨噬细胞、NK细胞功能下降，补体系统不健全，人类原代癌症和肿瘤很容易在其体内成癌症和肿瘤 ). GFP expression was maintained in the tumour cells the control SUM149 tumours were strictly noninvasive, as shown by their confinement within fibrotic capsules (A, B). miR-10b-overexpressing SUM149 tumours displayed a massive desmoplastic reaction, with islands of epithelial cancer cells that had invaded the stroma (C, D). apparent muscular and vascular invasion (E, F) 苏木素-伊红染色 Ki-67 proliferation marker MECA-32 endothelial cell marker. To determine whether miR-10b expression in the primary tumours would also affect cell proliferation and tumour angiogenesis, the distribution, but not the total number, of Ki-671 cells in the miR-10b-overexpressing SUM149 tumours was distinct from that seen in the control tumours Quantification of Ki-67 staining (percentage of Ki-671 carcinoma cells among total carcinoma cells; e) and vessels (using MECA-32-stained sections; f) at the centre and the edge of the SUM149 tumours. n53 mice at 6 weeks after implantation. Prominent intratumoural vessels are associated with the invasion front of miR-10b-overexpressing tumours as demonstrated by MECA-32 staining of primary mammary tumours formed by SUM149 cells infected with the miR-10b-expressing or empty vector, 5.1 miR-10b? cell migration and invasion in vitro 5.2 miR-10b ? tumour invasion in vivo 5.3 miR-10b ? distant metastasis in vi