5-Aza-dC ([[Decitabine]]) treatment combines with anti-[[PD-1]] immunotherapy to efficiently suppress the progression of GL261 gliomas. Data support a mechanism of [[epigenetic modifications]] of [[AP-2α]] that contributes to [[tumor immune evasion]], and reactivation of AP-2α synergizes with anti-PD-1 antibodies to increase [[antitumor]] efficacy, which may be a broadly applicable strategy in [[solid tumor]]s
((Long S, Huang G, Ouyang M, Xiao K, Zhou H, Hou A, Li Z, Zhong Z, Zhong D, Wang Q, Xiang S, Ding X. Epigenetically modified AP-2α by DNA methyltransferase facilitates glioma immune evasion by upregulating PD-L1 expression. Cell Death Dis. 2023 Jun 17;14(6):365. doi: 10.1038/s41419-023-05878-x. PMID: 37330579.))
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Guo et al. showed that [[Transforming growth factor Beta]] induced the downregulation of [[MST1]] expression in U87 and U251 glioma cells. Treatment of glioma cells with the DNA methylation inhibitor [[Decitabine]] (5-aza-2'-deoxycytidine 5-AzadC) prevented the loss of MST1 expression. Addition of 5-AzadC also reduced the TGF-β-stimulated proliferation, migration and invasiveness of glioma cells. Furthermore, Knockdown of [[DNMT1]] upregulated MST1 expression in gliomas cells. In addition, the inhibition of DNMT1 blocked TGF-β-induced proliferation, migration and invasiveness in glioma cells. These results suggest that TGF-β promotes glioma malignancy through DNMT1-mediated loss of MST1 expression
((Guo Z, Li G, Bian E, Ma CC, Wan J, Zhao B. TGF-β-mediated repression of MST1
by DNMT1 promotes glioma malignancy. Biomed Pharmacother. 2017 Aug 9;94:774-780. 
doi: 10.1016/j.biopha.2017.07.081. [Epub ahead of print] PubMed PMID: 28802229.
)).