ライフサイエンスコーパス: 5-aza-2'-deoxycytidine

1 lated tumour cell lines after treatment with 5-aza 2-deoxycytidine.

2 recovered in tumour cell lines treated with 5-aza 2-deoxycytidine.

3 n and could be restored after treatment with 5-aza-2-deoxycytidine.

4 reast tumour cell lines after treatment with 5'-aza-2'deoxycytidine.

5 ion, which was restored after treatment with 5-aza 2'-deoxycytidine.

6 fter inhibition of DNA methyltransferases by 5-aza-2'-deoxycytidine.

7 orated into viral DNA following reduction to 5-aza-2'-deoxycytidine.

8 ly elicited by demethylation agents, such as 5-Aza-2'-deoxycytidine.

9 be reactivated by the hypomethylating agent 5-aza-2'-deoxycytidine.

10 tin A, or a DNA methyltransferase inhibitor, 5-Aza-2'-deoxycytidine.

11 and reactivated by the demethylating agent, 5-aza-2'-deoxycytidine.

12 ell lines with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine.

13 d was reactivated by the demethylating agent 5-aza-2'-deoxycytidine.

14 fter treatment with a methylation inhibitor, 5-aza-2'-deoxycytidine.

15 ion with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine.

16 ed by treatment with DNA-demethylating agent 5-aza-2'-deoxycytidine.

17 ine xenografts by systemic administration of 5-aza-2'-deoxycytidine.

18 ssion are induced by the demethylating agent 5-aza-2'-deoxycytidine.

19 after treatment with the demethylating agent 5-Aza-2'-deoxycytidine.

20 east cancer cells with a demethylating agent 5-aza-2'-deoxycytidine.

21 ved by chemically induced demethylation with 5-aza-2'-deoxycytidine.

22 econstituted when cells were pretreated with 5-aza-2'-deoxycytidine.

23 iated cells with the DNA demethylating agent 5-aza-2'-deoxycytidine.

24 locus, was induced following treatment with 5-aza-2'-deoxycytidine.

25 significantly by treatment of the cells with 5-aza-2'-deoxycytidine.

26 after treatment with the demethylating agent 5-aza-2'-deoxycytidine.

27 after treatment with the demethylating agent 5-aza-2'-deoxycytidine.

28 sts treated with the DNA demethylating agent 5-aza-2'-deoxycytidine.

29 F-7 breast cancer cells synergistically with 5-aza-2'-deoxycytidine.

30 tro treatment with the hypomethylating agent 5-aza-2'-deoxycytidine.

31 r treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine.

32 sure to AH or by the DNA demethylating agent 5-aza-2'-deoxycytidine.

33 r cell line with the DNA demethylating agent 5-aza-2'-deoxycytidine.

34 lated glioma cell lines after treatment with 5-aza-2'-deoxycytidine.

35 vated by the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine.

36 et gene for RAs and the demethylation agent, 5-aza-2'-deoxycytidine.

37 expressed in cell lines after treatment with 5'-aza-2'-deoxycytidine.

38 peutic potential of the demethylating agent, 5'-aza-2'-deoxycytidine.

39 es; furthermore, the DNA demethylating agent 5 aza-2'deoxycytidine (5-Aza-dC) antagonizes the effects

40 However, treatment with 5'-aza-2'-deoxycytidine (5'-aza-dC) restored IGFBP-3 exp

41 that treatment with the demethylating agent 5'-aza-2'-deoxycytidine (5-Aza-dC) significantly inhibit

42 Treatment with 5'-aza-2'-deoxycytidine (5-azaC), a DNA methyltransferas

43 sociated with gene silencing, treatment with 5'-aza-2-deoxycytidine (5'-aza-dC) (an inhibitor of DNA

44 RNA (6-fold) in human HCC cells treated with 5'aza-2'deoxycytidine (5-Aza-CdR, DNA methylation inhibi

45 reatment with epigenetic silencing modifiers 5-aza-2'-deoxycytidine (5-aza) and trichostatin A (TSA).

46 uated whether the DNA methylation inhibitor, 5-aza-2'-deoxycytidine (5-Aza) could modulate extracellu

47 ner with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza), 0 of 14 mice developed p

48 ), and of HCT-116 colonocytes incubated with 5-aza-2'-deoxycytidine (5-AZA).

49 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) and the histone deace

50 DNA methylation inhibitors such as 5-aza-2'-deoxycytidine (5-Aza-CdR) are currently used fo

51 d to use DNA methylation inhibitors, such as 5-aza-2'-deoxycytidine (5-Aza-CdR) in attempts to reacti

52 PTX with the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-aza-CdR) induced higher levels

53 mor cell lines MDA-MB-231 and UACC 1179 with 5-aza-2'-deoxycytidine (5-aza-CdR) induced transcription

54 The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) inhibits DNA methyltr

55 and Molt 3, with the methylation inhibitor, 5-aza-2'-deoxycytidine (5-aza-CdR) resulted in increased

56 5-Aza-2'-deoxycytidine (5-aza-CdR), an inhibitor of DNA

57 Treatment of prostate cancer cell lines with 5-aza-2'-deoxycytidine (5-Aza-CdR), an inhibitor of DNA

58 Decitabine, or 5-aza-2'-deoxycytidine (5-aza-CdR), is a well-characteri

59 Treatment with 5-aza-2'-deoxycytidine (5-Aza-CdR), previously known for

60 ysiological levels to low doses of the DNMTi 5-aza-2'-deoxycytidine (5-aza-CdR), there is a synergist

61 t was decreased by the methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

62 ncer cell lines with the methylase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

63 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

64 tic target of methylation inhibitors such as 5-Aza-2'-deoxycytidine (5-Aza-CdR).

65 The nucleoside analog 5-aza-2'-deoxycytidine (5-aza-CdR, decitabine) is a pote

66 ment of these cells with demethylating agent 5-aza-2'-deoxycytidine (5-aza-dC) increased mRNA levels

67 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) increases the expressi

68 5-Aza-2'-deoxycytidine (5-aza-dC) is a nucleoside analog

69 with the DNA demethylating nucleoside analog 5-AZA-2'-deoxycytidine (5-AZA-dC) synergistically augmen

70 , showed induction of ABCG2 expression after 5-aza-2'-deoxycytidine (5-aza-dC) treatment, suggesting

71 ponents was restored with either IFNgamma or 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

72 on dependency of silencing was determined by 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

73 , treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine (5-Aza-dC) was sufficient to reac

74 We thus determined the role of 5-aza-2'-deoxycytidine (5-Aza-dC), an inhibitor of DNA m

75 ore, treatment with the demethylating agent, 5-Aza-2'-deoxycytidine (5-Aza-dC), restored TSP-1 expres

76 CRC) cell lines with or without treatment of 5-aza-2'-deoxycytidine (5-aza-dC).

77 nes with the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-aza-dC).

78 iminate use of demethylating agents, such as 5-aza-2'-deoxycytidine (5-Aza-dC).

79 east cancer cells with demethylating agents [5-aza-2'-deoxycytidine (5-aza-dC)] and histone deacetyla

80 A (TSA), a histone deacetylase inhibitor, or 5-aza-2'-deoxycytidine (5-AzaC), a DNA methyltransferase

81 aP(CS) and PC-3 with the demethylating agent 5-aza-2'-deoxycytidine (5-AZAdC) reactivated PMP24 mRNA

82 by methylation, the DNA demethylating agent 5-aza-2'-deoxycytidine (5-AZAdC) was assessed.

83 /activated status induced in normal cells by 5-aza-2'-deoxycytidine (5-azadC) was mimicked by conditi

84 l human bronchial epithelial cells following 5-aza-2'-deoxycytidine (5-azadC), Depsipeptide FK228 (DP

85 sing nucleoside analogs of cytosine, such as 5-aza-2'-deoxycytidine (5-azadC).

86 Treatment of cells with 5-aza-2'deoxycytidine (5-aza-dC) increases CDKN2A expres

87 The DNA methyltransferase inhibitor, 5-Aza-2'deoxycytidine (5-AzaCdR) is an approved epigenet

88 Treatment with either 5-Aza-2-deoxycytidine (5-Aza) or trichostatin A (TSA) wa

89 fter treatment with trichostatin A (TSA) and 5-Aza-2-deoxycytidine (5-Aza).

90 ated with a DNA methyltransferase inhibitor, 5-Aza-2-deoxycytidine (5-Aza-2dC), and an RAW294.7 cell

91 The DNA-demethylating drug 5-Aza-2-deoxycytidine (5-azadC) induced rapid nuclear ac

92 which have no detectable TFPI-2 expression, 5-aza-2'-deoxycytidine (5aC), an inhibitor of DNA methyl

93 permethylated genes following treatment with 5'-aza 2'-deoxycytidine (5Aza-dC).

94 reduction of DNMT with either the inhibitor 5-aza-2'-deoxycytidine (5Aza) or siRNA markedly reduced

95 after treatment with the demethylating agent 5-aza-2'-deoxycytidine (5Aza-dC) and/or the histone deac

96 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5Aza-dC) rapidly reduced Lys-9 m

97 r, the use of DNA-demethylating agents (e.g. 5-aza-2'-deoxycytidine (5aza-dC)) to study epigenetic re

98 eously immortal Li-Fraumeni fibroblasts with 5-aza-2'-deoxycytidine (5AZA-dC), an inhibitor of DNA me

99 upled it with a cell based loss-of-function (5-Aza-2'-deoxycytidine (5Aza-dC)-induced senescence bypa

100 Demethylation treatment with 5-aza-2'-deoxycytidine (5aza2dc) increased the sensitivi

101 xpressing reduced gamma-catenin protein with 5-aza-2'-deoxycytidine (5aza2dc), a DNA methylation inhi

102 5-Aza-2'-deoxycytidine (5azaC-dR) has been employed as a

103 4+ cells with the chromatin-modifying agents 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA),

104 ) cells with the chromatin-modifying agents, 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA).

105 DNA methyltransferase inhibitor, decitabine [5-aza-2'-deoxycytidine (5azaD)], followed by the histone

106 ut not normal CD34(+) cells with decitabine (5-aza-2'-deoxycytidine [5azaD]), followed by suberoylani

107 rone (DHT) and the DNA methylation inhibitor 5'-aza-2'-deoxycytidine (5AzadC) were introduced into th

108 5-Aza-2'-deoxycytidine (5azadC) inhibits DNA methyltrans

109 ls with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5azadC).

110 the AM cell line (MHS) after treatment with 5-aza-2'-deoxycytidine (a methyltransferase inhibitor).

111 press Lhx3 (Pit-1/0 cells) were treated with 5-aza-2'-deoxycytidine, a demethylating reagent.

112 Treatment with 5-aza-2'-deoxycytidine, a demethylation agent, and knock

113 Our reporter assays and gene reactivation by 5-aza-2'-deoxycytidine, a DNA demethylating agent, show

114 Expression of RASSF1A was restored with 5-aza-2'-deoxycytidine, a DNA methylation inhibitor.

115 s of tetradecanoyl phorbol acetate (TPA) and 5-aza-2'-deoxycytidine, a DNA methyltransferase inhibito

116 In vitro methylation of MAO B promoter with 5-aza-2'-deoxycytidine, a DNA methyltransferase inhibito

117 Treatment with 5-aza-2'-deoxycytidine, a methyltransferase inhibitor, c

118 yltransferase inhibitors, 5'-azacytidine and 5'-aza-2'-deoxycytidine, activated basal expression leve

119 h the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (ADC) to reactivate DNA methylati

120 ce treated with the DNA demethylating agent, 5-aza-2'-deoxycytidine, after UVB exposure.

121 with 10 muM DNA-methyltransferase inhibitor 5-aza-2'-deoxycytidine, again correlating with increased

122 ptide or the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine alone or concomitantly did not re

123 that manipulating MGPC DNA methylation with 5-aza-2'-deoxycytidine altered their properties.

124 antly, treatment of immortal cell lines with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransf

125 reduced LIF responsiveness were treated with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransf

126 Treatment with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransf

127 bination of DNA methyl transferase inhibitor 5-Aza 2-deoxycytidine and histone deacetylase inhibitor

128 after treatment with the demethylating drug 5-aza-2 deoxycytidine and histone deacetylation inhibiti

129 ot CXCR4 or SOX17, was strongly inhibited by 5-aza-2'-deoxycytidine and by knockdown of DNMT3b.

130 5-Aza-2'-deoxycytidine and diesel exhaust particle expos

131 ation and histone deacetylation because both 5-aza-2'-deoxycytidine and trichostatin A partially resc

132 demonstrating that promoter demethylation by 5-aza-2'-deoxycytidine and trichostatin A reactivated TI

133 is, we identified >160 genes up-regulated by 5-aza-2'-deoxycytidine and trichostatin A treatment.

134 cell line UACC3199 following treatment with 5-aza-2'-deoxycytidine and trichostatin A.

135 reatment with the DNA methylation inhibitors 5-aza-2'-deoxycytidine and zebularine as well as DNA met

136 Treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine and/or the histone deacetylase in

137 l lines with the methyltransferase inhibitor 5-aza-2-deoxycytidine and the histone deacetylase inhibi

138 and Jurkat) before and after treatments with 5-aza-2-deoxycytidine and trichostatin A.

139 etic repression of PDLIM2 can be reversed by 5-aza-2-deoxycytidine and vitamin D to suppress KSHV-ass

140 ed when Neuro2A cells were demethylated with 5-aza-2'-deoxycytidine, and increasing Sp3 levels in Sch

141 DNA-hypomethylating agents 5-azacytidine and 5-aza-2'-deoxycytidine are effective treatments for pati

142 ed by treatment with the demethylating agent 5-aza-2'-deoxycytidine as well as by down-modulation of

143 te using the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (Aza) induced acetylation of hist

144 0.01) increase in expression after 2 days of 5-aza-2'-deoxycytidine (AZA) treatment and a significant

145 ecific genetic Xist ablation with short-term 5-aza-2'-deoxycytidine (Aza) treatment models the synerg

146 Our purpose was to investigate whether 5-aza-2'-deoxycytidine (Aza), a DNA methyltransferase (D

147 Treatment with 5-aza-2'-deoxycytidine (AZA), a DNA methyltransferase in

148 s natively methylated, and subjected them to 5-aza-2'-deoxycytidine (Aza-C) treatment.

149 shock, but rather by the demethylating agent 5-aza-2'-deoxycytidine (Aza-C).

150 but not hexamethylene bisacetamide (HMBA) or 5-aza-2'-deoxycytidine (Aza-CdR), reactivate latent HIV-

151 d selectively bind to genomic DNA containing 5-aza-2'-deoxycytidine (aza-dC) in vivo.

152 The DNA methylation inhibitor, 5-aza-2'-deoxycytidine (aza-dC) increases collagen gene

153 MIS increases p16 protein levels, and 5'-Aza-2'-deoxycytidine (AzadC) induces p16 mRNA; theref

154 treatment, and combined treatment of TSA and 5-aza-2'-deoxycytidine (AzadC) synergistically induced e

155 B cells with the methyltransferase inhibitor 5-aza-2'-deoxycytidine before and at early stages of rep

156 The addition of 5-aza-2'-deoxycytidine blocked the hypoxia-induced incre

157 could be enhanced by treatment of cells with 5-aza-2'-deoxycytidine but not DMSO or retinoic acid.

158 permethylated, and the DNA methylation agent 5'-aza-2'-deoxycytidine, but not the histone deacetylase

159 ls with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine, caused a dramatic increase in KI

160 Treatment of cells with 5-aza-2'-deoxycytidine causes restoration of Cosmc trans

161 and treatment with the methylation inhibitor 5-Aza-2'-deoxycytidine could partially restore ASIC2 exp

162 460 lung cancer cells mediated by sequential 5-aza 2'-deoxycytidine (DAC)/depsipeptide FK228 (DP) exp

163 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (DAC) activates CYP24A1 expressio

164 eating lung cancer cell lines using low-dose 5-aza-2'-deoxycytidine (DAC) caused an accumulation of p

165 s cancer, we used the DNA demethylating drug 5-aza-2'-deoxycytidine (DAC) in an aggressive mouse mode

166 5-aza-2'-deoxycytidine (DAC) is approved for the treatme

167 hese cell lines with the demethylating agent 5-aza-2'-deoxycytidine (DAC) up-regulated SOCS-1 express

168 Treatment with a demethylating agent, 5-aza-2'-deoxycytidine (DAC), restored IL-6 induction of

169 0 cell line with the DNA demethylating agent 5-aza-2'-deoxycytidine (DAC)-enhanced HER4 expression, c

170 combination with the DNA-demethylating agent 5-aza-2'-deoxycytidine (DAC).

171 enocarcinoma cell lines after treatment with 5-aza-2'-deoxycytidine (DAC).

172 5 in cancer cells by three epigenetic drugs: 5-aza-2'-deoxycytidine (DAC; decitabine), arsenic trioxi

173 ation experiments of two CC cell lines using 5-aza-2'deoxycytidine (DAC) treatment.

174 lines treated with the methylation inhibitor 5-aza-2'deoxycytidine (DAC), where we found a 1-16% decr

175 cted a phase 1/2 study of the combination of 5-aza-2'-deoxycytidine (decitabine) and the histone deac

176 n in AML cell lines and patient blasts using 5-aza-2'-deoxycytidine (decitabine) and trichostatin A i

177 The cytidine analogues azacytidine and 5-aza-2'-deoxycytidine (decitabine) are commonly used to

178 s by 5-azacytidine (Vidaza) and its congener 5-aza-2'-deoxycytidine (decitabine) has provided an alte

179 The cytosine analog 5-aza-2'-deoxycytidine (decitabine) hypomethylates DNA b

180 The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (decitabine) induces DNA demethyl

181 5-Aza-2'-deoxycytidine (decitabine) is postulated to hav

182 Lung cancer cells are sensitive to 5-aza-2'-deoxycytidine (decitabine) or midostaurin (PKC4

183 e CpG island methylation, and treatment with 5-aza-2'-deoxycytidine (decitabine) resulted in up-regul

184 , led to widespread use of 5-azacytidine and 5-aza-2'-deoxycytidine (Decitabine) to demonstrate the c

185 the efficacy of arsenic trioxide (As2O3) or 5-aza-2-deoxycytidine (decitabine) alone and in combinat

186 Treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine decreased cell proliferation, gro

187 ce with low doses of the demethylating agent 5-aza-2'-deoxycytidine decreased the incidence of neopla

188 5-Aza-2'-deoxycytidine decreased, whereas folate-deplete

189 Sequential 5-aza-2'deoxycytidine/depsipeptide FK228 treatment marke

190 chromatin modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X expression in huma

191 Treatment of NPD cell lines with 5-aza-2'-deoxycytidine enhanced the expression of the pa

192 Furthermore, the DNA demethylating agent 5-aza-2-deoxycytidine failed to upregulate GAS5-AS1 in N

193 after treatment of cells with retinoic acid, 5-aza-2'-deoxycytidine, folate-depleted/high-methionine

194 Last, sequential treatment with 5-aza-2'-deoxycytidine followed by zebularine hindered t

195 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine for 5 days restored TIG1 expressi

196 sing ChIP-chip analysis, Trichostatin A, and 5-aza-2'-deoxycytidine further support an epigenetically

197 However, 5-aza-2'-deoxycytidine had no effect on the inflammatory

198 Treatment with 5'-aza-2'-deoxycytidine in a murine bleomycin-induced pu

199 macologic inhibition of DNA methylation with 5-aza-2'-deoxycytidine in combination with restoration o

200 These sites were screened by treatment with 5-aza-2'-deoxycytidine in four TN and five non-TNBC cell

201 or, Bob1 (OCA-B, OBF-1), were reactivated by 5-aza-2'-deoxycytidine, indicating that gene silencing i

202 evels in BT549 and MDA-MB-231 cells, whereas 5'-aza-2'-deoxycytidine induced expression in MDA-MB-231

203 Treatment with the DNA hypomethylating agent 5-aza-2'-deoxycytidine induced and up-regulated the mRNA

204 Treatment of cells with 30 mumol/L 5-aza-2'-deoxycytidine induced Gal-3 mRNA and protein ex

205 methylation, rather than genomic deletion as 5-aza-2'-deoxycytidine induced reactivation of DLC-1 exp

206 onexpressing cells and of T-cell clones with 5-aza-2'deoxycytidine induced IL-1alpha expression in th

207 The DNA methylase inhibitor, 5-aza-2'-deoxycytidine, induced KIR DNA hypomethylation

208 of AtT20 cells with the demethylating agent, 5-Aza-2'-deoxycytidine, induced the re-expression of thi

209 Moreover, zebularine and 5-aza-2-deoxycytidine, inhibitors of DNMT activity, bloc

210 Decitabine (5-aza-2'-deoxycytidine) inhibits DNA methylation and has

211 therapy, the demethylating drug decitabine (5-aza-2'-deoxycytidine) is increasingly used to treat ac

212 One such molecule is 5,6-dihydro-5-aza-2'-deoxycytidine (KP1212), a selective mutagen tha

213 Treatment of HepG2 cells with 5-aza-2'-deoxycytidine led to partial demethylation of t

214 of DNA methyltransferase (Dnmt) enzymes with 5-aza-2'-deoxycytidine or genetic ablation of both Dnmt1

215 ferentiated cells, exposure of DAOY cells to 5-aza-2'-deoxycytidine or their growth as stem cell-like

216 sed and hypomethylated genes, treatment with 5-aza-2'-deoxycytidine or with trichostatin A, either al

217 ld also be induced by a demethylating agent (5'-aza-2'-deoxycytidine) or histone deacetylase inhibito

218 Treatment with methylation (5-aza-2'-deoxycytidine) or deacetylation (trichostatin A

219 d with inhibition of methylation with either 5-Aza-2-Deoxycytidine, or siRNA to DNA Methyltransferase

220 Treatment with 5-aza-2'-deoxycytidine partially reactivated ARHI expres

221 (GSK126), or the DNA methylation inhibitor, 5-Aza-2'-deoxycytidine, partially restored miR-34a level

222 vation of the methylation-dependent genes by 5-aza-2'-deoxycytidine plus trichostatin A revealed a fu

223 upregulated by DNA demethylation induced by 5-aza-2'-deoxycytidine plus trichostatin A treatment and

224 ent with the DNA methyltransferase inhibitor 5'-aza-2'-deoxycytidine promoted demethylation of the OP

225 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine rapidly decreased the level of H3

226 tin A, but not the DNA methylation inhibitor 5'-aza-2'-deoxycytidine, re-established the expression o

227 y the data that demethylation of promoter by 5-aza-2'-deoxycytidine reactivated Betaig-h3 and restore

228 vitro treatment with the demethylating agent 5-aza-2'-deoxycytidine reactivated CRBP1 expression.

229 n and treatment with the demethylating agent 5-aza-2'-deoxycytidine reactivated SLIT2 gene expression

230 linical samples (P=0.004) and treatment with 5-aza-2'-deoxycytidine reactivated Spry2 expression in L

231 tment of KYSE220 ESCC and BIC EAC cells with 5-aza-2'-deoxycytidine reduced NELL1 methylation and inc

232 h the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine reduces cytosine methylation of t

233 l lines treated with the demethylating agent 5-AZA-2'-deoxycytidine reexpressed IGFBP3 at the mRNA an

234 melanoma cells with the demethylating agent 5-aza-2'-deoxycytidine reinduces Rap1GAP expression, fol

235 unoglobulin G (anti-IgG), and, surprisingly, 5-aza-2'-deoxycytidine require short exposures of 15 min

236 DEC with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored calcitriol-mediated indu

237 The demethylating agent 5-aza-2'-deoxycytidine restored caspase-8 expression and

238 Treatment with 5-aza-2'-deoxycytidine restored CDH13 expression in meth

239 Treatment with 5-aza-2'-deoxycytidine restored expression; dense methyl

240 xposure to the chromatin demethylating agent 5-aza-2'-deoxycytidine restored HSPA1A expression.

241 eatment of SMCs with the demethylating agent 5-aza-2'-deoxycytidine restored MCT3 expression and norm

242 nes with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored PDLIM2 expression and re

243 Treatment with 5-aza-2'-deoxycytidine restored RA response in two of th

244 Exposure to the demethylating agent 5-aza-2'-deoxycytidine restored RASSF1A expression, whil

245 whereas the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored the down-regulation of E

246 In vitro treatment of NK cells with 5-aza-2'-deoxycytidine restored the IL-2 signaling pathw

247 cells and treatment with demethylating agent 5-aza-2-deoxycytidine restored DOC2B expression.

248 cell lines with a DNA methylation inhibitor, 5-aza-2' deoxycytidine, restored hypoxia-induced BNIP3 e

249 ethylated at CpG islands, and treatment with 5'-aza-2'-deoxycytidine restores near-normal levels of m

250 ation by the DNA methyltransferase inhibitor 5'-aza-2'-deoxycytidine restores SP1 binding and STAT5A

251 Moreover, treatment with 5-aza-2'-deoxycytidine restores WIF-1 expression.

252 ersed by the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, restoring both SOD2 expression a

253 Treatment of myeloid cell lines with 5-aza-2'-deoxycytidine resulted in a significant decreas

254 tment of methylated/silenced cell lines with 5-aza-2'-deoxycytidine resulted in gene re-expression.

255 5-Aza-2'-deoxycytidine resulted in increased Cables expr

256 f the cell lines with the demethylating drug 5-aza-2'-deoxycytidine resulted in increased LXN express

257 Treatment of OV207 and SKOV3 by 5-aza-2'-deoxycytidine resulted in increased transcripti

258 Blocking methylation by treatment with 5-aza-2'-deoxycytidine resulted in reduced H3K4me3 bindi

259 Treatment with 5-Aza-2'-deoxycytidine resulted in restoration of gene t

260 Treatment with the demethylating agent 5-aza-2'-deoxycytidine resulted in TIMP-2 upregulation i

261 ression with the methyltransferase inhibitor 5-aza-2'deoxycytidine resulted in partial demethylation

262 ells with a DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine, resulted in lower methylation an

263 exon 1 hypermethylation, is re-expressed by 5-aza-2'deoxycytidine resulting in the restoration of a

264 d HBECs treated with the demethylating agent 5-aza-2'deoxycytidine revealed miR-196b and miR-34c-5p t

265 lls with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine reverses the methylation of the P

266 Decondensing the heterochromatin with 5-aza-2-deoxycytidine reverses the effects of ACF1 and S

267 eatment with the methyltransferase inhibitor 5-aza-2'-deoxycytidine, suggesting a role for DNA methyl

268 on1a and PLCepsilon1b by demethylating agent 5-aza-2'-deoxycytidine, suggesting epigenetic silencing

269 ated with a DNA methyltransferase inhibitor, 5-Aza-2'-Deoxycytidine, the APC expression in these cell

270 Upon extended growth in the absence of 5-aza-2'-deoxycytidine, the cells exhibit partial revers

271 SC-22 deregulation was reversed in vivo by a 5-aza-2'-deoxycytidine therapy of T or NK LGL leukemia,

272 ; when treated with the demethylating agent, 5-aza-2'-deoxycytidine, these five cell lines all showed

273 Combined with the induction of revertants by 5-aza-2'-deoxycytidine, this result suggested that stabi

274 We treated T24 bladder carcinoma cells with 5-Aza-2'-deoxycytidine to induce a transient demethylati

275 ted six cell lines lacking RASSF1A mRNA with 5-aza-2'deoxycytidine to examine the relationship betwee

276 )1 and DNMT3b3 proteins were undetectable in 5-Aza-2'-deoxycytidine-treated and untreated nondividing

277 We profiled mRNAs in control and 5-aza-2'-deoxycytidine-treated parents and allotetraploi

278 -G transcriptional activity was dependent of 5-aza-2'-deoxycytidine treatment and enhanced by interfe

279 tumors and cancer cell lines but induced by 5-aza-2'-deoxycytidine treatment in a dose-dependant man

280 We show that 5-aza-2'-deoxycytidine treatment not only reactivates ge

281 WIF1 re-expression upon 5-aza-2'-deoxycytidine treatment or WIF1 gene transfer i

282 ypomethylation of these promoters induced by 5-aza-2'-deoxycytidine treatment reactivated or enhanced

283 the ALF promoter inhibits activity and that 5-aza-2'-deoxycytidine treatment reactivates the endogen

284 The 5-aza-2'-deoxycytidine treatment restored MB-COMT expres

285 5-aza-2'-deoxycytidine treatment resulted in demethylati

286 Gene expression analyses and 5-aza-2'-deoxycytidine treatment showed that promoter hy

287 tion in 25% to 93% of the HNSCC samples, and 5-aza-2'-deoxycytidine treatment was able to restore exp

288 C tumor samples, and DNA demethylation using 5-aza-2'-deoxycytidine treatment was able to significant

289 5-Aza-2'-deoxycytidine treatment, bisulfite DNA sequenci

290 s DNA demethylated and reexpressed following 5-aza-2'-deoxycytidine treatment, H3K9me1 and H3K9me2 ar

291 After 5-aza-2'-deoxycytidine treatment, increased expression o

292 ced HLA-G transcriptional activity following 5-aza-2'-deoxycytidine treatment.

293 (n = 15) and 9% of NSCLCs (n = 11), whereas 5-aza-2'deoxycytidine treatment restored CAV1 expression

294 gastric cancer (IGC) cell lines treated with 5-aza-2'-deoxycytidine using microarrays containing 22,2

295 Importantly, when 5-aza-2'-deoxycytidine was combined with the histone dea

296 lowing treatment with a demethylating agent, 5-aza-2'-deoxycytidine, was shown.

297 Using 5-aza-2'-deoxycytidine, we show that DNA methylation is

298 The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, which inhibits DNA methylation,

299 lls with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, which reduced DNA methylation fr

300 Treating Jurkat T cells with 5-aza-2'-deoxycytidine, which reduced DNA methylation, i