学科主题临床医学
Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo
Yu, Weidong1,3; Sun, Xiaolin1; Clough, Nancy4,5; Cobos, Everardo1,2; Tao, Yunxia1; Dai, Zonghan1,2
刊名CARCINOGENESIS
2008-09-01
DOI10.1093/carcin/bgn098
29期:9页:1717-1724
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
资助者National Institutes of Health/National Cancer Institute ; National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases ; National Institutes of Health/National Cancer Institute ; National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases
研究领域[WOS]Oncology
关键词[WOS]CHRONIC MYELOID-LEUKEMIA ; CHRONIC MYELOGENOUS LEUKEMIA ; HOMOLOGY 3 DOMAIN ; UNDERLYING ABNORMAL TRAFFICKING ; BINDING-PROTEIN ; MALIGNANT PROGENITORS ; DEPENDENT DEGRADATION ; TRANSFORMING ACTIVITY ; INTERACTING PROTEIN ; TYROSINE KINASES
英文摘要

Abl interactor (Abi) 1 was first identified as the downstream target of Abl tyrosine kinases and was found to be dysregulated in leukemic cells expressing oncogenic Bcr-Abl and v-Abl. Although the accumulating evidence supports a role of Abi1 in actin cytoskeleton remodeling and growth factor/receptor signaling, it is not clear how it contributes to Bcr-Abl-induced leukemogenesis. We show here that Abi1 gene silencing by short hairpin RNA attenuated the Bcr-Abl-induced abnormal actin remodeling, membrane-type 1 metalloproteinase clustering and inhibited cell adhesion and migration on fibronectin-coated surfaces. Although the knock down of Abi1 expression did not affect growth factor-independent growth of Bcr-Abl-transformed Ba/F3 cells in vitro, it impeded competitive expansion of these cells in non obese diabetic (NOD)/ severe combined immuno-deficiency (SCID) mice. Remarkably, the knock down of Abi1 expression in Bcr-Abl-transformed Ba/F3 cells impaired the leukemogenic potential of these cells in NOD/SCID mice. Abi1 contributes to Bcr-Abl-induced leukemogenesis in part through Src family kinases, as the knock down of Abi1 expression attenuates Bcr-Abl-stimulated activation of Lyn. Together, these data provide for the first time the direct evidence that supports a critical role of Abi1 pathway in the pathogenesis of Bcr-Abl-induced leukemia.

语种英语
所属项目编号R01 CA094921 ; K01 DK067191
资助者National Institutes of Health/National Cancer Institute ; National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases ; National Institutes of Health/National Cancer Institute ; National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases
WOS记录号WOS:000258961200007
引用统计
被引频次:21[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66214
专题北京大学第二临床医学院_临床分子生物学研究所
作者单位1.Texas Tech Univ, Hlth Sci Ctr, Dept Internal Med, Amarillo, TX 79106 USA
2.Texas Tech Univ, Hlth Sci Ctr, Stem Cell Transplant Program, Amarillo, TX 79106 USA
3.Peking Univ, Peoples Hosp, Inst Clin Mol Biol, Beijing 100044, Peoples R China
4.Univ Colorado Denver, Div Med Oncol, Aurora, CO 80010 USA
5.Hlth Sci Ctr, Aurora, CO 80010 USA
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GB/T 7714
Yu, Weidong,Sun, Xiaolin,Clough, Nancy,et al. Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo[J]. CARCINOGENESIS,2008,29(9):1717-1724.
APA Yu, Weidong,Sun, Xiaolin,Clough, Nancy,Cobos, Everardo,Tao, Yunxia,&Dai, Zonghan.(2008).Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo.CARCINOGENESIS,29(9),1717-1724.
MLA Yu, Weidong,et al."Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo".CARCINOGENESIS 29.9(2008):1717-1724.
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