S100A9 is a mediator of the ID1 functions in metastasis

Metastasis is a major factor responsible for mortality in breast cancer patients. Id1 plays important roles in cell differentiation and promotes tumor angiogenesis, cell invasion and metastasis. Although Id1 is established as a critical factor for lung metastasis in breast cancer, the pathways and molecular mechanisms of Id1 functions in metastasis remains to be defined. Here we show that Id1 interacts with TFAP2A to suppress S100A9 expression. The expression of Id1 and S100A9 is inversely correlated in both breast cancer cell lines and clinical samples. We also find that S100A9 expression rescues the migratory and invasive phenotypes in vitro and metastasis in vivo induced by Id1 expression. S100A9 also suppresses the expression of known metastasis promoting factor RhoC activated by Id1 expression. Our results suggest that S100A9 mediates the functions of Id1 in breast cancer metastasis. MCF7 cell lines under three conditions: control, Id1 overexpression, Id2 overexpression. Each condition has 2 replicates