The extracellular matrix in breast cancer

被引:323
作者
Insua-Rodriguez, Jacob [1 ,2 ]
Oskarsson, Thordur [1 ,2 ,3 ]
机构
[1] Heidelberg Inst Stem Cell Technol & Expt Med HI S, Neuenheimer Feld 280, D-69120 Heidelberg, Germany
[2] German Canc Res Ctr, Cell Biol & Tumor Biol Program, D-69120 Heidelberg, Germany
[3] German Canc Consortium DKTK, Heidelberg, Germany
关键词
Extracellular matrix; Breast cancer; Metastasis; Niche; Therapy; PLASMINOGEN-ACTIVATOR SYSTEM; LEUCINE-RICH PROTEOGLYCANS; CARCINOMA IN-SITU; SYNDECAN-1; EXPRESSION; DUCTAL CARCINOMA; BONE METASTASIS; GENE-EXPRESSION; TUMOR INVASION; UP-REGULATION; CATHEPSIN-K;
D O I
10.1016/j.addr.2015.12.017
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The extracellular matrix (ECM) is increasingly recognized as an important regulator in breast cancer. ECM in breast cancer development features numerous changes in composition and organization when compared to the mammary gland under homeostasis. Matrix proteins that are induced in breast cancer include fibrillar collagens, fibronectin, specific laminins and proteoglycans as well as matricellular proteins. Growing evidence suggests that many of these induced ECM proteins play a major functional role in breast cancer progression and metastasis. A number of the induced ECM proteins have moreover been shown to be essential components of metastatic niches, promoting stem/progenitor signaling pathways and metastatic growth. ECM remodeling enzymes are also markedly increased, leading to major changes in the matrix structure and biomechanical properties. Importantly, several ECM components and ECM remodeling enzymes are specifically induced in breast cancer or during tissue regeneration while healthy tissues under homeostasis express exceedingly low levels. This may indicate that ECM and ECM-associated functions may represent promising drug targets against breast cancer, providing important specificity that could be utilized when developing therapies. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:41 / 55
页数:15
相关论文
共 234 条
[1]   Blockade of MMP14 Activity in Murine Breast Carcinomas: Implications for Macrophages, Vessels, and Radiotherapy [J].
Ager, Eleanor I. ;
Kozin, Sergey V. ;
Kirkpatrick, Nathaniel D. ;
Seano, Giorgio ;
Kodack, David P. ;
Askoxylakis, Vasileios ;
Huang, Yuhui ;
Goel, Shom ;
Snuderl, Matija ;
Muzikansky, Alona ;
Finkelstein, Dianne M. ;
Dransfield, Daniel T. ;
Devy, Laetitia ;
Boucher, Yves ;
Fukumura, Dai ;
Jain, Rakesh K. .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2015, 107 (04)
[2]   Thrombospondin-1 and transforming growth factor-beta1 promote breast tumor cell invasion through upregulation of the plasminogen/plasmin system [J].
Albo, D ;
Berger, DH ;
Wang, TN ;
Hu, XL ;
Rothman, V ;
Tuszynski, GP .
SURGERY, 1997, 122 (02) :493-499
[3]   Decorin Suppresses Bone Metastasis in a Breast Cancer Cell Line [J].
Araki, Kentaro ;
Wakabayashi, Hiroki ;
Shintani, Ken ;
Morikawa, Joji ;
Matsumine, Akihiko ;
Kusuzaki, Katsuyuki ;
Sudo, Akihiro ;
Uchida, Atsumasa .
ONCOLOGY, 2009, 77 (02) :92-99
[4]   Hyaluronan synthases (HAS1-3) in stromal and malignant cells correlate with breast cancer grade and predict patient survival [J].
Auvinen, Paivi ;
Rilla, Kirsi ;
Tumelius, Ritva ;
Tammi, Markku ;
Sironen, Reijo ;
Soini, Ylermi ;
Kosma, Veli-Matti ;
Mannermaa, Arto ;
Viikari, Jukka ;
Tammi, Raija .
BREAST CANCER RESEARCH AND TREATMENT, 2014, 143 (02) :277-286
[5]   Fibronectin expression in carcinoma cells correlates with tumor aggressiveness and poor clinical outcome in patients with invasive breast cancer [J].
Bae, Young Kyung ;
Kim, Aeri ;
Kim, Min Kyoung ;
Choi, Jung Eun ;
Kang, Su Hwan ;
Lee, Soo Jung .
HUMAN PATHOLOGY, 2013, 44 (10) :2028-2037
[6]   Cilengitide inhibits progression of experimental breast cancer bone metastases as imaged noninvasively using VCT, MRI and DCE-MRI in a longitudinal in vivo study [J].
Baeuerle, Tobias ;
Komljenovic, Dorde ;
Merz, Maximilian ;
Berger, Martin R. ;
Goodman, Simon L. ;
Semmler, Wolfhard .
INTERNATIONAL JOURNAL OF CANCER, 2011, 128 (10) :2453-2462
[7]   Epithelial to Mesenchymal Transition Promotes Breast Cancer Progression via a Fibronectin-dependent STAT3 Signaling Pathway [J].
Balanis, Nikolas ;
Wendt, Michael K. ;
Schiemann, Barbara J. ;
Wang, Zhenghe ;
Schiemann, William P. ;
Carlin, Cathleen R. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2013, 288 (25) :17954-17967
[8]   High syndecan-1 expression in breast carcinoma is related to an aggressive phenotype and to poorer prognosis [J].
Barbareschi, M ;
Maisonneuve, P ;
Aldovini, D ;
Cangi, MG ;
Pecciarini, L ;
Mauri, FA ;
Veronese, S ;
Caffo, O ;
Lucenti, A ;
Palma, PD ;
Galligioni, E ;
Doglioni, C .
CANCER, 2003, 98 (03) :474-483
[9]   Metastatic Growth from Dormant Cells Induced by a Col-I-Enriched Fibrotic Environment [J].
Barkan, Dalit ;
El Touny, Lara H. ;
Michalowski, Aleksandra M. ;
Smith, Jane Ann ;
Chu, Isabel ;
Davis, Anne Sally ;
Webster, Joshua D. ;
Hoover, Shelley ;
Simpson, R. Mark ;
Gauldie, Jack ;
Green, Jeffrey E. .
CANCER RESEARCH, 2010, 70 (14) :5706-5716
[10]   The syndecan-1 ectodomain regulates αvβ3 integrin activity in human mammary carcinoma cells [J].
Beauvais, DLM ;
Burbach, BJ ;
Rapraeger, AC .
JOURNAL OF CELL BIOLOGY, 2004, 167 (01) :171-181