Moreover, a transgenic mouse model demonstrated that CTCs returned to the primary tumor and generated new tumors with enhanced tumorigenic capacity.147 Mechanistic investigations demonstrated that overexpression of stromal-derived factor-1γ (SDF-1γ or CXCL12γ) induced CSC phenotypes in prostate cancer cells through CXCR4-mediated PKCα/NFκB signaling148 and Wnt signaling,147 which promoted tumor outgrowth, metastasis and chemoresistance in vivo. Here, CXCR4 is linked to neoplasm.