We uncovered the anti-metastatic potential of fisetin in cervical cancer cells and elucidated its molecular mechanism, that is fisetin inhibits the activation of p38 MAPK, impairs translocation of NF-κB to the nucleus, and then decreases its binding amounts on the promoter of uPA gene, and results in repressing the expression and activity of uPA, leading to disrupting the invasiveness and motility of cervical cancer cells (Figure 7). Here, NFKB1 is linked to cervical cancer.