Low-dose decitabine induces MAGE-A expression and inhibits invasion via suppression of NF-?B2 and MMP2 in Eca109 cells - 23/09/14
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Abstract |
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.
Le texte complet de cet article est disponible en PDF.Keywords : Decitabine, MAGE-A, Esophageal squamous cell carcinoma, Invasion, Immunotherapy
Abbreviations : ESCC, CTA, MAGE-A, RT-PCR, RNA, MTT
Plan
Vol 68 - N° 6
P. 745-750 - juillet 2014 Retour au numéro
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