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Laminin-332-rich tumor microenvironment for tumor invasion in the interface zone of breast cancer.

 Baek Gil Kim  ;  Hee Jung An  ;  Suki Kang  ;  Yoon Pyo Choi  ;  Ming-Qing Gao  ;  Haengran Park  ;  Nam Hoon Cho 
 AMERICAN JOURNAL OF PATHOLOGY, Vol.178(1) : 373-381, 2011 
Journal Title
Issue Date
Breast Neoplasms/genetics* ; Breast Neoplasms/pathology* ; Cadherins/genetics ; Cell Adhesion Molecules/genetics* ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Epithelial-Mesenchymal Transition/genetics ; Female ; Gene Expression Regulation, Neoplastic* ; Homeodomain Proteins/genetics ; Humans ; Integrin alpha6beta4/genetics ; Matrix Metalloproteinase 14/genetics ; MicroRNAs/genetics ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Neoplasm Invasiveness ; Snail Family Transcription Factors ; Transcription Factors/genetics ; Tumor Microenvironment* ; Zinc Finger E-box-Binding Homeobox 1
Dense fibrosis, which is caused by desmoplastic reaction, is usually found in invasive ductal carcinoma and may represent the alteration of the tumor microenvironment preceding tumor invasion. Thus, the dense fibrotic zone around invasive ductal carcinoma can be considered to be the actual tissue site of tumor microenvironment, where the precedent alterations for tumor invasion occur. To characterize the dense fibrotic zone, we classified invasive ductal carcinoma tissue into a tumor zone, a normal zone, and the novel interface zone (IZ), which shows dense fibrosis. The postulated IZ is a 5-mm-wide belt that circles the tumor margin and overlaps with normal tissue. Of the extracellular matrix components, laminin-332 was specifically overexpressed in the IZ. Events that appear to be similar to the epithelial-mesenchymal transition, a novel source of myofibroblast formation from epithelial cells, were observed in the IZ, according to the following characteristics: overexpression of matrix metalloproteinase 3, membrane type 1-matrix metalloproteinase, snail, and zinc finger E-box-binding homeobox 1, and the gain of N-cadherin expression, as well as the down-regulation of miR200c. The myofibroblasts isolated from the IZ, which were designated interface zone-fibroblast, displayed laminin-332 and membrane type 1-matrix metalloproteinase overexpression, in contrast with both cancer-associated fibroblasts and normal breast fibroblasts. Taken together, our results suggest that the IZ, which shows dense fibrosis, may provide a specialized microenvironment for guiding tumor invasion: the fibrosis caused by laminin-332 overexpressing myofibroblast formation (interface zone-fibroblast) via epithelial-mesenchymal transition.
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1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kang, Suki(강숙희) ORCID logo https://orcid.org/0000-0002-9957-3479
Gao, Ming Qing(고명청)
Kim, Baek Gil(김백길) ORCID logo https://orcid.org/0000-0001-6270-1433
Park, Haeng Ran(박행란)
Cho, Nam Hoon(조남훈) ORCID logo https://orcid.org/0000-0002-0045-6441
Choi, Yoon Pyo(최윤표)
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