Decitabine, a demethylating drug, is the first-line treatment for 
myelodysplastic syndromes and gains better overall survival, which is based on 
epigenetic mechanism. Activated by promoter demethylation, melanoma-associated 
antigens-A (MAGE-A), cancer-testis antigens are attractive targets for 
immunotherapy. Our purpose was to investigate whether decitabine could show 
anti-tumor effects for esophageal cancer and explore its mechanism. In addition, 
we aimed to examine its modulation for most MAGE-A members. The results showed 
the baseline expression were MAGE-A2, -3,-9, and -10 in Eca109 cells and 
decitabine (0.5 μM) could induce MAGE-A8 and -A4 whereas reduce MAGE-A9 and 
-A10. Moreover, decitabine (0.5 μM) inhibited cell proliferation, migration and 
invasive ability by 15%, 34% and 47.2%, respectively and decreased expressions 
of NF-κB2 and MMP2. Our results demonstrated that low-dose decitabine induced 
the expression of MAGE-A8 and -A4, and inhibited cell invasion through 
decreasing expression of MMP2 and NF-κB2, which provides possibilities for 
combing decitabine with immunotherapy targeting MAGE-A to treat advanced 
esophageal squamous cell carcinoma.