Journal Article

Genomic Instability of Human Mammary Epithelial Cells Overexpressing a Truncated Form of EMSY

Afshin Raouf, Lindsay Brown, Nikoleta Vrcelj, Karen To, Winnie Kwok, David Huntsman and Connie J. Eaves

in JNCI: Journal of the National Cancer Institute

Volume 97, issue 17, pages 1302-1306
Published in print September 2005 | ISSN: 0027-8874
Published online September 2005 | e-ISSN: 1460-2105 | DOI: http://dx.doi.org/10.1093/jnci/dji254
Genomic Instability of Human Mammary Epithelial Cells Overexpressing a Truncated Form of EMSY

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The EMSY gene encodes a protein that interacts with Brca2 and is amplified in some sporadic cases of human breast cancer. To examine whether overexpression of EMSY would mimic the chromosome instability phenotype that is associated with the loss of Brca2 function, we constructed a lentiviral vector (Lenti-EMSY/GFP) that encodes a truncated form of the Emsy protein, including its Brca2-interacting domain, and green fluorescent protein (GFP) and used it to transduce human telomerase-immortalized human breast epithelial (184-hTert) cells, which have a nearly normal karyotype. At passage 5 after transduction, 39 (26%) of 150 EMSY/GFP-transduced metaphase cells contained at least one structural chromosomal abnormality compared with 19 (13%) of 150 GFP-transduced metaphase cells (P = .003, chi-square test); at passage 10, the corresponding frequencies were 42% and 15%, respectively (P<.001). Mitomycin C also produced a severalfold higher frequency of chromosome breaks in the EMSY/GFP-transduced cells than in the control cells. These results support the hypothesis that EMSY overexpression can play a role in the genesis of human breast cancer.

Journal Article.  2818 words.  Illustrated.

Subjects: Medical Oncology

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