Tumor cell-organized fibronectin maintenance of a dormant breast cancer population

被引:89
作者
Barney, Lauren E. [1 ]
Hall, Christopher L. [1 ]
Schwartz, Alyssa D. [1 ]
Parks, Akia N. [2 ]
Sparages, Christopher [1 ]
Galarza, Sualyneth [1 ]
Platt, Manu O. [2 ]
Mercurio, Arthur M. [3 ]
Peyton, Shelly R. [1 ]
机构
[1] Univ Massachusetts, Dept Chem Engn, Amherst, MA 01003 USA
[2] Emory Univ, Wallace H Coulter Dept Biomed Engn, Georgia Inst Technol, Atlanta, GA 30332 USA
[3] Univ Massachusetts, Dept Mol Cell & Canc Biol, Med Sch, Worcester, MA 01605 USA
基金
美国国家卫生研究院; 美国国家科学基金会;
关键词
BONE-MARROW; EXTRACELLULAR-MATRIX; METASTASIS; SURVIVAL; MECHANISMS; ADHESION; ALPHA-5-BETA-1; FIBROBLASTS; INTEGRINS; SUBSTRATE;
D O I
10.1126/sciadv.aaz4157
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Tumors can undergo long periods of dormancy, with cancer cells entering a largely quiescent, nonproliferative state before reactivation and outgrowth. To understand the role of the extracellular matrix (ECM) in regulating tumor dormancy, we created an in vitro cell culture system with carefully controlled ECM substrates to observe entrance into and exit from dormancy with live imaging. We saw that cell populations capable of surviving entrance into long-term dormancy were heterogeneous, containing quiescent, cell cycle-arrested, and actively proliferating cells. Cell populations capable of entering dormancy formed an organized, fibrillar fibronectin matrix via alpha(v)beta(3 )and alpha(5)beta(1) integrin adhesion, ROCK-generated tension, and TGF beta 2 stimulation, and cancer cell outgrowth after dormancy required MMP-2-mediated fibronectin degradation. We propose this approach as a useful, in vitro method to study factors important in regulating dormancy, and we used it here to elucidate a role for fibronectin deposition and MMP activation.
引用
收藏
页数:12
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