Mammary Cancer and Activation of Transposable Elements
Abstract
The purpose of this project is to investigate molecular events of the preclinical stages of mammary cancer, specifically, the intersection between the development of genome demethylation, retrotransposon transcriptional activity, and retrotransposon-driven transcription of cellular genes in an engineered parity-dependent mouse model of mammary cancer. These inbred mice develop mammary cancer after 3 litters. Mammary epithelial cells (MEC) were isolated from cancer-prone and control mice after 1 or 3 litters. DNA and RNA were isolated from the MEC. Data from Illumina HiSeq RNA libraries was forwarded to our collaborator Dr John Edwards for transcriptome analysis. DNA from MEC was sent to Dr Edwards for processing and methylome analysis. As expected, using Methyl-MAPS analysis, Dr Edwards identified whole genome hypomethylation in tumor-prone MEC compared with controls after 3 litters. We did not identify increased retrotransposon expression. An unexpected and intriguing observation was upregulated expression of immune system suppressors in tumor-prone MEC after 3 litters. Wet lab independent confirmation of the findings is pending, and forms part of the research plan for a doctoral student in Adelaide. Our data suggest that while hypomethylation is an early event in this model, upregulated retrotransposon expression is a later event, and unlikely to play a direct role in cancer ontogeny.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2015
- Accession Number
- AD1001608
Entities
People
- Anne Peaston
Organizations
- University of Adelaide