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Basal-like breast cancers (BLBCs) express genes characteristic of myoepithelial/basal cells in the normal mammary gland and comprise up to 25% of all breast cancers. Chemotherapy is the only systemic therapy for BLBC, which preferentially affects younger women and African-American women, and is associated with high histological grade, aggressive clinical behavior, and a propensity to metastasize to the brain and lung. To date, little is known about the molecular basis of BLBC. We have found that the FOXC1 transcription factor, which is involved in embryonic development, is a critical biomarker for BLBC. FOXC1 overexpression induces breast cancer cell growth, migration, invasion, and chemoresistance. We are now using cell models to identify the signaling pathways mediating the effect of FOXC1 on BLBC cell functions. We also exploit mouse models to determine whether FOXC1 regulates BLBC development in vivo and predisposes breast cancer to brain and lung metastasis. Furthermore, we intend to define the molecular mechanisms responsible for upstream regulation of FOXC1 overexpression in basal-like breast cancer.By providing insight into the signaling mechanism for FOXC1 regulation of breast cancer cell function, this study will advance our understanding of BLBC development and facilitate establishing a critical functional marker for detection and diagnosis of BLBC. Results may warrant development and clinical investigation of agents that block FOXC1. Finally, understanding how FOXC1 expression is regulated may allow development of FOXC1-based strategies to prevent BLBC.
We also found that several other genes, which are normally found in brain tissue, are overexpressed in breast cancer. We are using cell and mouse models to address whether these genes predispose breast cancer cells to brain metastasis.