Mechanistically, due to the combination of HDAC10 and the promoters of MMP-2 (especially the AP1-binding site) and MMP-9 (especially the NF-κB- and sp1-binding sites) the decreased level of histone acetylation impedes the binding function of polymerase II, weakens the expression levels of MMP-2 and MMP-9 and restrains cancer cell invasion and migration [53]. Here, HDAC10 is linked to cancer.