Figure 3.

A schematic model depicting how CAP1 likely regulates the FAK/ERK axis and Rap1, and through these, controls invasiveness and proliferation in metastatic breast cancer cells. Knockdown of CAP1 activates FAK, and which in turn activates ERK. The activated ERK and Rap1 lead to elevated cell proliferation. On the other hand, enhanced cell adhesion and increased turnover of focal adhesions from activated FAK and Rap1, as well as the activated ERK/Snail/E-Cadherin signals may collectively stimulate cancer cell invasiveness, and overcome negative effects on cancer cell invasiveness from the reduced rate of actin filament turnover, due to the loss of CAP1 function in these cells. The cell signals that function in cohort to control transient phosphorylation at the S307/S309 tandem regulatory site on CAP1 likely control the cancer cell functions through CAP1.