BP1 Regulates PI3K/Akt Pathway by Targeting Vascular Endothelial Growth Factor (VEGF) in Breast Cancer
1. Department of Medicine (Division of Genomic Medicine), and Department of Microbiology, Immunology and Tropical Medicine, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA
2. Affiliated Minda Hospital of Hubei University of Nationalities, Enshi, Hubei 445000, China
3. Department of Medicine (Division of Hematology/Oncology), The George Washington University School of Medicine and Health Sciences, Washington, DC, USA
The progression of breast cancer has been linked to a splice variant of DLX4 homeobox transcription factor called BP1, which is overexpressed in 81% of primary breast cancer. Our ChIP-on-chip and bioinformatic analysis studies showed that VEGFA is a potential target of BP1, and it is upregulated in cells overexpressing BP1. VEGFA has been implicated in tumor generation because it stimulates angiogenesis, proliferation, and migration. This study aims to decipher the functional roles of BP1 in VEGFA-PI3K/AKT pathways in tumorigenesis, using an estrogen receptor (ER) negative breast cancer cell line, Hs578T. QPCR and Western blots were performed on three overexpressing and two vector control cell lines to assess and compare the transcriptional and translational expression. Our findings illustrate the increased expression of VEGFA, pPI3K, and pAkt when BP1 is overexpressed. Therefore, BP1 may play an important role in regulating the PI3K/Akt pathway through VEGFA.
Keywords: breast cancer, BP1, VEGFA and PI3K