个人中心| | 帮助
高级检索
当前位置： 首页 > 详情页

Molecular Checkpoint Decisions Made by Subverted Vascular Niche Transform Indolent Tumor Cells into Chemoresistant Cancer Stem Cells.

| 认领 | 导出 | |

文献详情

资源类型：

收录情况： ◇ 自然指数

作者：
Zhongwei Cao[1,2] ; Joseph M. Scandura[3] ; Giorgio G. Inghirami[4] ; Koji Shido[1] ; Bi-Sen Ding[1,2] ; Shahin Rafii[1] ;
机构： [1]Division of Regenerative Medicine, Department of Medicine, Ansary Stem Cell Institute, Weill Cornell Medicine, New York, NY 10065, USA [2]Laboratory of Birth Defects and Related Diseases of Women and Children, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu 610041, China [3]Division of Hematology-Oncology, Department of Medicine [4]Department of Pathology and Laboratory Medicine Weill Cornell Medicine, New York, NY 10065, USA
出处：
DOI： 10.1016/j.ccell.2016.11.010
ISSN：

关键词： angiocrine factors cancer stem cells chemoresistance ETS2 IGFBP7/angiomodullin insulin growth factor-1 tumor aggressiveness tumor endothelial cell tumor microenvironment vascular niche

摘要：
Tumor-associated endothelial cells (TECs) regulate tumor cell aggressiveness. However, the core mechanism by which TECs confer stem cell-like activity to indolent tumors is unknown. Here, we used in vivo murine and human tumor models to identify the tumor-suppressive checkpoint role of TEC-expressed insulin growth factor (IGF) binding protein-7 (IGFBP7/angiomodulin). During tumorigenesis, IGFBP7 blocks IGF1 and inhibits expansion and aggresiveness of tumor stem-like cells (TSCs) expressing IGF1 receptor (IGF1R). However, chemotherapy triggers TECs to suppress IGFBP7, and this stimulates IGF1R+ TSCs to express FGF4, inducing a feedforward FGFR1-ETS2 angiocrine cascade that obviates TEC IGFBP7. Thus, loss of IGFBP7 and upregulation of IGF1 activates the FGF4-FGFR1-ETS2 pathway in TECs and converts naive tumor cells to chemoresistant TSCs, thereby facilitating their invasiveness and progression. Copyright © 2017 Elsevier Inc. All rights reserved.

基金：
We are indebted to Dr. Michael Ginsberg at Angiocrine Bioscience for supplying mouse endothelial cells and Drs Dean W. Felsher and Stephanie C. Casey at Stanford University for kindly providing mouse HCC cells. We are grateful to Dr. Ralf Adams at Max Planck Institute and Dr. Michael Simons at Yale University for generously sharing Chd5(PAC)-CreERT2 and floxed Fgfr1 mice, respectively. We also thank Mr. Deebly Chavez for his assistance with animal procedure. Z.C. was supported by Druckenmiller Fellowship from the New York Stem Cell Foundation. J.M.S is supported by the Ansary Stem Cell Institute, Taub Foundation Grants Program for MDS Research, Tri-Institutional Stem Cell Initiative (TRI-SCI #2014-023 and #2016-024), Leukemia & Lymphoma Society grant 2299-14, the Empire State Stem Cell Board and New York State Department of Health grant (C029156, C030160, ECRIP-Empire Clinical Research Investigator Program), NIH R56-HL116436-01A1, Cancer Research and Treatment Fund (CR&T), and NIH R01 (HL119872, HL128158). G.G.I. is supported by the Italian Association for Cancer Research (AIRC) Special Program in Clinical Molecular Oncology, Milan (5x1000 No. 10007) and by the SCOR Leukemia Lymphoma Society Grant (2015 Translational Discovery in Peripheral T-Cell Lymphomas). K.S. is supported by the Ansary Stem Cell Institute, the starr foundation TRI-Institution stem cell core project, the Empire State Stem Cell Board and New York State Department of Health grants (C026878, C028117, C029156, C030160). B-S.D. was supported by a National Scientist Development grant from the American Heart Association (12SDG1213004) and National Heart, Lung, and Blood Institute R01HL130826-01. S.R. is supported by Ansary Stem Cell Institute, the Starr Foundation TRI-Institution Stem Cell core project, Tri-Institutional Stem Cell Initiative (TRI-SCI #2013-032, #2014-023, #2016-013), the Empire State Stem Cell Board and New York State Department of Health grants (C026878, C028117, C029156, C030160, ECRIP-Empire Clinical Research Investigator Program), and by grants from the NIH R01 HL099997 and U54 CA163167. S.R. is the founder and non-paid consultant to Angiocrine Bioscience, New York, NY.
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2017]版：
大类 | 1 区 医学
小类 | 1 区 细胞生物学 1 区 肿瘤学
最新[2023]版：
大类 | 1 区 医学
小类 | 1 区 细胞生物学 1 区 肿瘤学
第一作者：
第一作者机构： [1]Division of Regenerative Medicine, Department of Medicine, Ansary Stem Cell Institute, Weill Cornell Medicine, New York, NY 10065, USA [2]Laboratory of Birth Defects and Related Diseases of Women and Children, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu 610041, China
通讯作者：
通讯机构： [1]Division of Regenerative Medicine, Department of Medicine, Ansary Stem Cell Institute, Weill Cornell Medicine, New York, NY 10065, USA [2]Laboratory of Birth Defects and Related Diseases of Women and Children, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu 610041, China
推荐引用方式(GB/T 7714)：
Zhongwei Cao,Joseph M. Scandura,Giorgio G. Inghirami,et al.Molecular Checkpoint Decisions Made by Subverted Vascular Niche Transform Indolent Tumor Cells into Chemoresistant Cancer Stem Cells.[J].Cancer cell.2017,31(1):110-126.doi:10.1016/j.ccell.2016.11.010.
APA：
Zhongwei Cao,Joseph M. Scandura,Giorgio G. Inghirami,Koji Shido,Bi-Sen Ding&Shahin Rafii.(2017).Molecular Checkpoint Decisions Made by Subverted Vascular Niche Transform Indolent Tumor Cells into Chemoresistant Cancer Stem Cells..Cancer cell,31,(1)
MLA：
Zhongwei Cao,et al."Molecular Checkpoint Decisions Made by Subverted Vascular Niche Transform Indolent Tumor Cells into Chemoresistant Cancer Stem Cells.".Cancer cell 31..1(2017):110-126

相关文献

[1]Molecular Checkpoint Decisions Made by Subverted Vascular Niche Transform Indolent Tumor Cells into Chemoresistant Cancer Stem Cells. [2]Endothelium originated from colorectal cancer stem cells constitute cancer blood vessels. [3]Higher IGFBP-1 to IGF-1 serum ratio predicts unfavourable survival in patients with nasopharyngeal carcinoma [4]Cancer and stem cells. [5]Endothelium originated from colorectal cancer stem cells constitute cancer blood vessels. [6]The expression difference of insulin-like growth factor 1 receptor in breast cancers with or without diabetes. [7]Low-temperature 3D-printed collagen/chitosan scaffolds loaded with exosomes derived from neural stem cells pretreated with insulin growth factor-1 enhance neural regeneration after traumatic brain injury [8]Long non-coding RNAs: Emerging regulators for chemo/immunotherapy resistance in cancer stem cells. [9]Bone Angiogenesis and Vascular Niche Remodeling in Stress, Aging, and Diseases. [10]PCK1 attenuates tumor stemness via activating the Hippo signaling pathway in hepatocellular carcinoma

资源点击量：46424 今日访问量：0 总访问量：3323 更新日期：2024-11-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 四川省肿瘤医院 技术支持：重庆聚合科技有限公司 地址：成都市人民南路四段55号