CXCR4 and neoplasm: Ateeq et al. showed that 5-aza-2′-deoxycytidine (5-aza-CdR) reactivated the tumor suppressor RASSF1A and inhibited tumor growth in non-invasive breast cancer cells, but simultaneously upregulated prometastatic genes (uPA, CXCR4, heparanase, SNCG, VEGF, TGF-β) through promoter demethylation, enhancing invasion and migration both in vitro and in vivo [172].