Mechanistically, a lower level of miR-7 expression existed in prostate cancer cells than in non-tumorigenic prostate epithelial cells, resulting in an over-expression of miR-7, which suppressed the stemness and tumorigenesis properties of PCSCs by targeting the KLF4/PI3K/AKT/p21 pathways (85). Here, AKT1 is linked to prostate cancer.