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Retinoic acid nuclear receptor β inhibits breast carcinoma anchorage independent growth
Author(s) -
Li XiaoSu,
Shao ZhiMing,
Sheikh M. Saeed,
Eiseman Julie L.,
Sentz Dorothy,
Jetten Anton M.,
Chen JianChyi,
Dawson Marcia I.,
Aisner Seena,
Rishi Arun K.,
Gutierrez Peter,
Schnapper Lauren,
Fontana Joseph A.
Publication year - 1995
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041650302
Subject(s) - retinoic acid , transfection , retinoic acid receptor , biology , cell growth , cell culture , microbiology and biotechnology , receptor , nuclear receptor , cancer research , biochemistry , gene , transcription factor , genetics
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.