The miR-200 and miR-221/222 microRNA Families: Opposing Effects on Epithelial Identity

  • Erin N. Howe
  • Dawn R. Cochrane
  • Jennifer K. Richer
Article

DOI: 10.1007/s10911-012-9244-6

Cite this article as:
Howe, E.N., Cochrane, D.R. & Richer, J.K. J Mammary Gland Biol Neoplasia (2012) 17: 65. doi:10.1007/s10911-012-9244-6

Abstract

Carcinogenesis is a complex process during which cells undergo genetic and epigenetic alterations. These changes can lead tumor cells to acquire characteristics that enable movement from the primary site of origin when conditions become unfavorable. Such characteristics include gain of front-rear polarity, increased migration/invasion, and resistance to anoikis, which facilitate tumor survival during metastasis. An epithelial to mesenchymal transition (EMT) constitutes one way that cancer cells can gain traits that promote tumor progression and metastasis. Two microRNA (miRNA) families, the miR-200 and miR-221 families, play crucial opposing roles that affect the differentiation state of breast cancers. These two families are differentially expressed between the luminal A subtype of breast cancer as compared to the less well-differentiated triple negative breast cancers (TNBCs) that exhibit markers indicative of an EMT. The miR-200 family promotes a well-differentiated epithelial phenotype, while high miR-221/222 results in a poorly differentiated, mesenchymal-like phenotype. This review focuses on the mechanisms (specific proven targets) by which these two miRNA families exert opposing effects on cellular plasticity during breast tumorigenesis and metastasis.

Keywords

miR-200 miR-221 miR-222 EMT MET Breast cancer 

Abbreviations

EMT

Epithelial to mesenchymal transition

ZEB1/2

Zinc finger E-box binding homeobox 1/2

UTR

Untranslated Region

MET

Mesenchymal to epithelial transition

MDCK

Madin-Darby Canine Kidney

iPSC

Induced pluripotent stem cell

TGF-β

Transforming growth factor beta

PDGF

Platelet derived growth factor

EGFR

Epidermal growth factor receptor

NCI

National Cancer Institute

VEGF

Vascular endothelial growth factor

ER

Estrogen receptor

MMTV

Murine mammary tumor virus

TRPS1

trichorhinophalangeal 1

PLZF

promyelocytic leukemia zinc finger

Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Erin N. Howe
    • 1
    • 2
  • Dawn R. Cochrane
    • 2
  • Jennifer K. Richer
    • 1
    • 2
  1. 1.Program in Cancer BiologyUniversity of ColoradoAuroraUSA
  2. 2.Department of PathologyUniversity of ColoradoAuroraUSA

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