Loss of canonical Smad4 signaling promotes KRAS driven malignant transformation of human pancreatic duct epithelial cells and metastasis.
第一作者:
Lisa,Leung
第一单位:
Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada ; Ontario Cancer Institute/Princess Margaret Hospital, and University Health Network, University of Toronto, Toronto, Ontario, Canada.
作者:
医学主题词
动物(Animals);癌, 胰腺管(Carcinoma, Pancreatic Ductal);细胞系, 肿瘤(Cell Line, Tumor);细胞转化, 肿瘤(Cell Transformation, Neoplastic);上皮细胞(Epithelial Cells);基因表达调控, 肿瘤(Gene Expression Regulation, Neoplastic);基因敲低技术(Gene Knockdown Techniques);基因沉默(Gene Silencing);人类(Humans);小鼠(Mice);肿瘤侵润(Neoplasm Invasiveness);肿瘤转移(Neoplasm Metastasis);胰腺管(Pancreatic Ducts);原癌基因蛋白质类(Proto-Oncogene Proteins);原癌基因蛋白质类p21(ras)(Proto-Oncogene Proteins p21(ras));RNA, 小分子干扰(RNA, Small Interfering);信号传导(Signal Transduction);Smad4蛋白质(Smad4 Protein);存活率分析(Survival Analysis);转化生长因子β(Transforming Growth Factor beta);ras蛋白质类(ras Proteins)
DOI
10.1371/journal.pone.0084366
PMID
24386371
发布时间
2021-10-21
- 浏览9
PloS one
e84366页
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