Fig. 7

RAC1 restores the MDA-MB-231 cell tumor forming ability that is lost from RAB4A knockdown in the orthotopic mammary fat pad mice model. A The formation and growth of tumors derived from control MDA-MB-231 cells, and those with stable RAB4A knockdown alone or concurrent RAB4A knockdown and RAC1 overexpression. The analysis was performed using Prism software. The numbers of mice in each experimental group are: RAB4A KD, 10 mice (RAB4A KD#1 and RAB4A KD#2 includes 5 mice each); combined RAB4A KD with concurrent expression of wild-type RAC1, 10 mice (RAB4A KD#1 + RAC1^WT and RAB4A KD#2 + RAC1^WT includes 5 mice each); combined RAB4A KD with concurrent expression of constitutive active RAC1, 10 mice (RAB4A KD#1 + RAC1^CA and RAB4A KD#2 + RAC1^CA includes 5 mice each); control shRNA group, 15 mice. The growth curves of the ten RAB4A KD and ten RAB4A KD + RAC1^WT all fall onto the X-axis; the solid red diamond and open purple diamond represent these two groups, respectively. B Graphic illustration of the proposed model based on the study results. RAB4A-RAC1 signaling is an essential regulatory pathway of EMT, invasion and stemness, which are critical features of cancer progression. RAB4A acts through integrin β3 to control the activation of RAC1