Electronic Thesis/Dissertation
 

BP1 Regulates PI3K/Akt Pathway through Activation of VEGF

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The progression of breast cancer has been linked to a splice variant of DLX4 homeobox transcription factor, 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, we believe that BP1 plays an important role in regulating the PI3K/Akt pathway through VEGFA.

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