Myoepithelial Cells: Autocrine and Paracrine Suppressors of Breast Cancer Progression

  • Sanford H. BarskyEmail author
  • Nina J. Karlin


Host cellular paracrine regulation of tumor progression is an important determinant of tumor biology but one cell that has been ignored in this regulation is the myoepithelial cell. Myoepithelial cells surround normal ducts and precancerous lesions, especially of the breast and form a natural border separating proliferating epithelial cells from proliferating endothelial cells (angiogenesis). Myoepithelial cells may thus negatively regulate tumor invasion and metastasis. Whereas epithelial cells are susceptible targets for transforming events, myoepithelial cells are resistant. Therefore, it can be said that myoepithelial cells function as both autocrine as well as paracrine tumor suppressors. Our laboratory has found that myoepithelial cells secrete a number of suppressor molecules including high amounts of diverse proteinase inhibitors and angiogenic inhibitors but low amounts of proteinases and angiogenic factors compared to common malignant cell lines. This observation has been made in vitro, in mice, and in humans and suggests that myoepithelial cells exert pleiotropic suppressive effects on tumor progression. The gene expression profile of myoepithelial cells may explain the pronounced anti-invasive and anti-angiogenic effects of myoepithelial cells on carcinoma cells and may also account for the reduced malignancy of myoepithelial tumors, which are devoid of appreciable angiogenesis and invasive behavior.

Key Words

myoepithelial cells tumor suppression expression profile angiogenic inhibitors proteinase inhibitors 

Abbreviations used


acidic fibroblast growth factor


alpha 1-antitrypsin




basic fibroblast growth factor


common acute lymphocytic leukemia antigen


chloramphenicol acetyl transferase


comparative genomic hybridization


type I collagen α1 chain


type IV collagen α1 chain


type IV collagen α2 chain


conditioned medium


N6,2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate


ductal carcinoma in situ


ductal lavage fluid






estrogen receptor-α


estrogen receptor-β


fetal calf serum




heparin-binding endothelial cell growth factor


hepatocyte growth factor


hypoxia-inducible factor-alpha


human mammary epithelial cells


hypoxia response element


hormone replacement therapy




inducible nitric oxide synthase


keratinocyte serum-free medium


loss of heterozygosity


matrix metalloproteinase-9




sodium butyrate


plasminogen activator inhibitor-1


platelet-derived endothelial cell growth factor


placental growth factor


phorbol 12-myristate 13-acetate: PN-II, protease nexin-II


all trans retinoic acid


tissue inhibitor of metalloproteinase-1


transforming growth factor α


transforming growth factor β


tumor necrosis factor α


human umbilical vein endothelial cells


urokinase-type plasminogen activator


vascular endothelial growth factor


von Willebrand factor


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Copyright information

© Springer Science + Business Media, Inc. 2006

Authors and Affiliations

  1. 1.Department of PathologyThe Ohio State University College of MedicineColumbus
  2. 2.Department of Medicine, Division of Hematology-OncologyUCLA-Olive View Medical CenterSylmar
  3. 3.Department of PathologyThe Ohio State University College of MedicineColumbus

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