Open AccessThe LIM domain gene LMO4 inhibits differentiation of mammary epithelial cells in vitro and is overexpressed in breast cancer
Author(s) -
Jane E. Visvader,
Deon J. Venter,
Kyungmin Hahm,
Margaret Santamaria,
Eleanor Y. M. Sum,
Lorraine A. O’Reilly,
David J. White,
Rachael Williams,
Jane E. Armes,
Geoffrey J. Lindeman
Publication year - 2001
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.251547698
Subject(s) - carcinogenesis , mammary gland , biology , cancer research , lim domain , epithelium , cellular differentiation , in situ hybridization , breast cancer , cell growth , microbiology and biotechnology , gene expression , gene , cancer , transcription factor , zinc finger , genetics
LMO4 belongs to a family of LIM-only transcriptional regulators, the first two members of which are oncoproteins in acute T cell leukemia. We have explored a role for LMO4, initially described as a human breast tumor autoantigen, in developing mammary epithelium and breast oncogenesis. Lmo4 was expressed predominantly in the lobuloalveoli of the mammary gland during pregnancy. Consistent with a role in proliferation, forced expression of this gene inhibited differentiation of mammary epithelial cells. Overexpression of LMO4 mRNA was observed in 5 of 10 human breast cancer cell lines. Moreover, in situ hybridization analysis of 177 primary invasive breast carcinomas revealed overexpression of LMO4 in 56% of specimens. Immunohistochemistry confirmed overexpression in a high percentage (62%) of tumors. These studies imply a role for LMO4 in maintaining proliferation of mammary epithelium and suggest that deregulation of this gene may contribute to breast tumorigenesis.
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