About the Project
Metastatic Breast Cancer is incurable. There is therefore an urgent need to develop therapies to prevent metastatic breast cancer. Our previous work has demonstrated that the Runx2 transcriptional co-activator, CBFb, is required for the expression of metastatic genes in breast cancer cells. The aim of this project is to determine the role of CBFb, in the formation of metastases and identify new therapeutic targets to prevent metastasis. The project uses ChIP-seq, RNA-seq and microarray technologies combined with novel 3-D cell co-culture systems to identify genes that promote metastasis in breast cancer.
Funding Notes
This project has a Band 3 fee. Details of our different fee bands can be found on our website. For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website. Informal enquiries may be made directly to the primary supervisor.
References
Mendoza-Villanueva, D., Zeef, L. & Shore, P (2011). Metastatic breast cancer cells inhibit osteoblast differentiation through the Runx2/CBFbeta-dependent expression of the Wnt antagonist, Sclerostin. Breast Cancer Res, 13(5), R106.
Deng W, Lopez-Camacho C Tang J-Y, Mendoza-Villanueva D, Maya-Mendoza, Jackson D.A, and Shore P. (2012). Cytoskeletal protein filamin A is a nucleolar protein that suppresses ribosomal RNA gene transcription. PNAS 109 (5), 1524.
Mendoza-Villanueva D, Deng W, Lopez-Camacho C, Shore P. (2010). The Runx transcriptional co-activator, CBFbeta, is essential for invasion of breast cancer cells. Molecular Cancer, 9(171),
Shore P. (2005). A role for Runx2 in normal mammary gland and breast cancer bone metastasis. Journal of cellular biochemistry, 96(3), 484-9.
Inman CK, Li N, Shore P. (2005). Oct-1 counteracts autoinhibition of Runx2 DNA binding to form a novel Runx2/Oct-1 complex on the promoter of the mammary gland-specific gene beta-casein. Molecular and Cellular Biology, 25(8), 3182-93.
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