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Cichon MA, Nelson CM, Radisky DC. Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion. Cancer Inform. 2015;14:1-13doi: 10.4137/CIN.S18965.
Cichon, M. A., Nelson, C. M., & Radisky, D. C. (2015). Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion. Cancer informatics, 141-13. https://doi.org/10.4137/CIN.S18965
Cichon, Magdalena A, et al. "Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion." Cancer informatics vol. 14 (2015): 1-13. doi: https://doi.org/10.4137/CIN.S18965
Cichon MA, Nelson CM, Radisky DC. Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion. Cancer Inform. 2015 Feb 09;14:1-13. doi: 10.4137/CIN.S18965. eCollection 2015. PMID: 25698877; PMCID: PMC4325704.
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Cancer Inform. 2015 Feb 09;14:1-13. doi: 10.4137/CIN.S18965. eCollection 2015.

Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion.

Cancer informatics

Magdalena A Cichon, Celeste M Nelson, Derek C Radisky

Affiliations

  1. Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL USA.
  2. Department of Chemical and Biological Engineering, Princeton University, Princeton, NJ, USA. ; Department of Molecular Biology, Princeton University, Princeton, NJ, USA.

PMID: 25698877 PMCID: PMC4325704 DOI: 10.4137/CIN.S18965

Abstract

Epithelial-mesenchymal transition (EMT) is a physiological program that is activated during cancer cell invasion and metastasis. We show here that EMT-related processes are linked to a broad and conserved program of transcriptional alterations that are influenced by cell contact and adhesion. Using cultured human breast cancer and mouse mammary epithelial cells, we find that reduced cell density, conditions under which cell contact is reduced, leads to reduced expression of genes associated with mammary epithelial cell differentiation and increased expression of genes associated with breast cancer. We further find that treatment of cells with matrix metalloproteinase-3 (MMP-3), an inducer of EMT, interrupts a defined subset of cell contact-regulated genes, including genes encoding a variety of RNA splicing proteins known to regulate the expression of Rac1b, an activated splice isoform of Rac1 known to be a key mediator of MMP-3-induced EMT in breast, lung, and pancreas. These results provide new insights into how MMPs act in cancer progression and how loss of cell-cell interactions is a key step in the earliest stages of cancer development.

Keywords: breast cancer; cell contact; epithelial-mesenchymal transition; extracellular matrix; mammary epithelial cells; matrix metalloproteinases

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