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. 2015 Oct 9;6:159. doi: 10.3389/fendo.2015.00159

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Copyright © 2015 Zhu and Zhou.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The regulation of VEGFR-2 in breast cancer cells. After the binding of VEGF to its cognate receptor VEGFR-2, VEGFR-2 activates STAT3 dimer formation. STAT3 dimer activates STAT3-response element (SRE)-containing genes, including MYC and SOX2 (top and lower right). MYC and SOX2 are embryonic stem cell transcription factors (ES-TF). They will affect many downstream EMT-related genes, such as up-regulating SNAIL, SLUG, ZEB1, and ZEB2 and down-regulating CDH1. These genes will endow the breast cancer cells the capability of cell motility and cancer stem cell self-renewal. Another exciting advance found that mutant p53, together with SWI/SNF histone remodeling complex, will be recruited to the VEGFR-2 promoter to activate VEGFR-2 in triple-negative breast cancer cell lines (lower left).