Volume 165, Issue 3 pp. 449-458
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Retinoic acid nuclear receptor β inhibits breast carcinoma anchorage independent growth

Xiao-Su Li

Xiao-Su Li

Department of Medicine, Division of Oncology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

University of Maryland, School of Medicine and the Veterans Administration Medical Center, Baltimore, Maryland 21201

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Zhi-Ming Shao

Zhi-Ming Shao

Department of Medicine, Division of Oncology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

University of Maryland, School of Medicine and the Veterans Administration Medical Center, Baltimore, Maryland 21201

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M. Saeed Sheikh

M. Saeed Sheikh

Department of Medicine, Division of Oncology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

University of Maryland, School of Medicine and the Veterans Administration Medical Center, Baltimore, Maryland 21201

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Julie L. Eiseman

Julie L. Eiseman

Departments of Pathology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

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Dorothy Sentz

Dorothy Sentz

Departments of Pathology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

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Anton M. Jetten

Anton M. Jetten

Cell Biology Section, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709

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Jian-Chyi Chen

Jian-Chyi Chen

Department of Medicine, Division of Oncology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

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Marcia I. Dawson

Marcia I. Dawson

Life Sciences Division, SRI International, Menlo Park, California 94025

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Seena Aisner

Seena Aisner

Departments of Pathology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

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Arun K. Rishi

Arun K. Rishi

Department of Medicine, Division of Oncology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

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Peter Gutierrez

Peter Gutierrez

Departments of Biochemistry, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

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Lauren Schnapper

Lauren Schnapper

Departments of Sugery, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

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Joseph A. Fontana

Corresponding Author

Joseph A. Fontana

Department of Medicine, Division of Oncology, Baltimore, Maryland 21201

Departments of Cancer Center, Baltimore, Maryland 21201

University of Maryland, School of Medicine and the Veterans Administration Medical Center, Baltimore, Maryland 21201

University of Maryland at Baltimore, Cancer Center, Room S9 D05, 22 S. Greene Street, Baltimore, Maryland 21201Search for more papers by this author
First published: December 1995
Citations: 37

Abstract

Retinoids modulate cellular proliferation and mediate gene function through a series of nuclear receptors. The retinoic acid nuclear receptor β (RARβ) plays an important role in the differentiation of a number of cell types. We now demonstrate that RARβ expresion is confined to normal mammary tissue and is not expressed in either immortalized normal or malignant cell lines. Treatment of RARβ-transfected MDA-MB-231 cells with 1 μM all-trans-retinoic acid (RA) significantly inhibited monolayer growth of the cells which express recombinant RARβ. RARβ-expressing MDA-MB-231 cells formed significantly smaller and fewer colonies soft agar than the mock-transfected cells. Addition of 1 μM RA stimulated colony size and number in the RARβ-transfected MDA-MB-231 cells. In contast to the RARβ-expressing cells, colony formation by the RARβ-expressing cells was similar to the mock-transfected controls and the addition of 1 μM RA to the RARα-transfected cells inhibited colony formation. While demonstrating decreased colony formation in agar, RARβ-expressing MDA-MB-231 cells failed to exhibit decreased growth in SCID mice. Our results show that RARβ functions as a negative regulator of growth in breast epithelial cells. In addition, the growth of these cells is differentially regulated by RARα and RARβ which is most likely the result to the modulation of different genes. © 1995 Wiley-Liss Inc.

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