ライフサイエンスコーパス: ZEB1

1 l markers (N-cadherin, Vimentin, Twist2, and ZEB1).

2 M) and zinc finger E-box binding homeobox 1 (ZEB1).

3 ssor of the established PPCD-associated gene ZEB1.

4 hose with low expression of p-PDGFRalpha and ZEB1.

5 scription factors JUN and SP1 in addition to ZEB1.

6 ts the growth of EGFR-mutated cells, induces ZEB1.

7 11, CCR4, PLCG1, CDKN2A, ARID1A, RPS6KA1 and ZEB1.

8 lly regulated by NF-kappaB and ZEB2, but not ZEB1.

9 , reciprocal regulation of EMT by UBQLN1 and ZEB1.

10 mparison of relative changes of Galpha12 and ZEB1.

11 er region, and demonstrate LIF repression by ZEB1.

12 metastatic disease due to high expression of ZEB1.

13 by their requirement for different levels of ZEB1.

14 expression of the transcriptional repressor ZEB1.

15 tion of EMT-promoting transcriptional factor Zeb1.

16 lture to target mesenchymal genes, including ZEB1.

17 invasion and metastasis, which is induced by ZEB1.

18 ess, including the upregulation of SNAI1 and ZEB1.

19 primarily via crosstalk with E-cadherin and ZEB1.

20 al polarity master genes via upregulation of ZEB1.

21 es these changes, as does silencing Slug and ZEB1.

22 A) mutant fails to elicit EMT and upregulate ZEB1.

23 PDGFRbeta through the direct suppression of ZEB1.

24 also Src inhibition reduced the induction of ZEB1.

25 expression, whereas cAMP markedly inhibited ZEB1/2 and TGF-beta.

26 sion of known targets, transcription factors ZEB1/2 and TGF-beta2.

27 invasion potential as a result of increased ZEB1/2 levels, which specifically suppress the anti-inva

28 equent stimulation of the MEK1/2-ERK1/2-Fra1-ZEB1/2 signaling pathway.

29 the expression of miR-205, which can silence ZEB1/2 to prevent the loss of epithelial character cause

30 ZEB1/2 upregulation by WASF3 results from downregulation

31 the expression of the miR-200b gene targets ZEB1/2, GATA2, and KDR was confirmed by qRT-PCR as being

32 finger and homeobox transcription factor-1 (Zeb1), a master regulator of epithelial polarity, contro

33 Luciferase reporter assays demonstrated that Zeb1, a crucial regulator of epithelial-to-mesenchymal t

34 om latency is dependent on the expression of Zeb1, a key regulator of the epithelial-to-mesenchymal t

35 sition (EMT) is activated in cancer cells by ZEB1, a member of the zinc finger/homeodomain family of

36 , miR-200 and miR-155, respectively regulate Zeb1, a repressor of Gnrh transcriptional activators and

37 IM and zinc finger E-box binding homeobox 1 (ZEB1), aberrant cell motility, and increased invasivenes

38 Only TAMs that expressed full levels of Zeb1 accelerated tumor growth.

39 nt animals and human lung cancer cell lines, ZEB1 activated PI3K by derepressing miR-200 targets, inc

40 nce of amplified collagen gene expression in ZEB1-activated mesenchymal lung cancer cells.

41 ZEB1 acts in a negative feedback loop to block expressio

42 iently form sarcomas in nude mice, and a Ras-ZEB1-Akt pathway then causes transition of these tumours

43 Collectively, our findings reveal Ovol-Zeb1-alpha-catenin sequential repression and highlight O

44 However, ZEB1 also represses cyclin-dependent kinase (cdk) inhibi

45 Moreover, ZEB1, an EMT activator and transcriptional repressor of

46 ZEB1 and activated PDGFRalpha were coexpressed in invasi

47 dicates that paclitaxel-induced reduction of ZEB1 and beta-tubulin isotypes are, in part, due to incr

48 Similarly, Elevated expression of ZEB1 and CD117 are found in the prostate basal cell popu

49 SPRR2a complexes with ZEB1 and CtBP on the microRNA (miR)-200c/141 promoter re

50 An inverse correlation between CD117 or ZEB1 and DAB2IP is also found in clinical specimens.

51 tly correlates with the transcription factor Zeb1 and is elevated in mesenchymal-like metastatic lung

52 In addition, we demonstrate that ZEB1 and ITGB4 are important in modulating the histopath

53 In concert with the effects of MUC1-C on ZEB1 and miR-200c, we show that MUC1-C induces EMT and c

54 and expression of beta-catenin, Snail, Slug, Zeb1 and N-cadherin, and upregulated E-cadherin.

55 Galpha12QL induced ZEB1 and other epithelial-mesenchymal transition markers

56 MT) phenotype characterized by expression of Zeb1 and Snail1.

57 5 overexpression inhibited CRIPTO1-dependent ZEB1 and SRC activation, restoring erlotinib sensitivity

58 ized genetic cell context-dependent role for ZEB1 and suggest that NOTCH1 may be a useful target for

59 findings indicate that (i) MUC1-C activates ZEB1 and suppresses miR-200c with the induction of EMT a

60 The co-ordinate upregulation of ZEB1 and suppression of miR-200c has been linked to the

61 Reciprocal modulation of ZEB1 and TCF4 activities involves their binding to DNA a

62 -205 inhibits DNA damage repair by targeting ZEB1 and the ubiquitin-conjugating enzyme Ubc13.

63 ns, and up-regulation of mesenchymal markers Zeb1 and Vim.

64 hat also expressed the "mesenchymal" markers ZEB1 and vimentin, whereas FGFR3 expression was restrict

65 EMT can be mediated by activation of the ZEB1 and ZEB2 (ZEB) transcription factors, which repress

66 wn MCF-7 cells consistently showed increased ZEB1 and ZEB2 expression and decreased E-cadherin expres

67 tin-1 and E2F1 on vimentin, fibronectin, and ZEB1 and ZEB2 promoters.

68 family of zinc finger transcription factors, ZEB1 and ZEB2, execute EMT programs in embryonic develop

69 ression of the mesenchymal genes, as well as ZEB1 and ZEB2, through the mediation of the E2F1 transcr

70 in and fibronectin as well as EMT regulators ZEB1 and ZEB2.

71 er, thereby downregulating its target genes, ZEB1 and ZEB2.

72 expression of miR-205 and its target genes, ZEB1 and ZEB2.

73 in lower expression of miR-200a target genes ZEB1 and ZEB2.

74 ciated transcriptional repressors, including ZEB1 and ZEB2.

75 ription factors (N-cadherin, Slug, Snail and Zeb1), and upregulation of E-cadherin.

76 ssociated with an increase in N-cadherin and Zeb1, and decrease in E-cadherin expression.

77 comprises the microRNA 200 (miR-200) family, ZEB1, and GRHL2.

78 n relationship between Ovol2 and EMT inducer Zeb1, and observed that adding this regulation generates

79 sed invasion and elevated the levels of VIM, ZEB1, and SLUG mRNAs.

80 Furthermore, the loss of Mel-18 promoted ZEB1- and ZEB2-mediated downregulation of E-cadherin tra

81 ated in feedback loops controlled by miRNAs, ZEB1 appears to be a central switch that determines cell

82 naling and EMT-inducing transcription factor ZEB1 are critical to mediate these effects of GM-CSF.

83 g and CD44 splicing pathways associated with ZEB1 are potential EMT chemoprevention and therapeutic t

84 chymal markers including Vimentin, Snail and ZEB1 are significantly elevated.

85 and late adipogenic regulators, identifying ZEB1 as a central transcriptional component of fat cell

86 These data establish ZEB1 as a key factor in the tumor microenvironment and f

87 iRNAs and mRNA changes enabled us to predict ZEB1 as a key molecule governed by Galpha12.

88 These findings implicate ZEB1 as a stem cell regulator in glioma which when delet

89 ion of zinc-finger E-box-binding homeobox 1 (ZEB1) as mediated by microRNA deregulation.

90 ic TFs and characterized the top ranking TF, ZEB1, as being essential for adipogenesis both in vitro

91 is the upregulation of the major EMT inducer ZEB1, as these effects are reversed by ZEB1 knock-down b

92 (LSK) cells shows dysregulated expression of ZEB1-associated genes involved in the small GTPase-depen

93 In turn, ZEB1 associates with MUC1-C and the ZEB1/MUC1-C complex

94 more, we found that p21 forms a complex with ZEB1 at the miR-183-96-182 cluster promoter to inhibit t

95 -regulatory transcription factors TWIST1 and ZEB1 attenuated mesothelial clearance in ovarian cancer

96 t regulation of LOX and LOXL2 by the miR-200/ZEB1 axis, defines a novel mechanism driving tumor metas

97 We identified ZEB1 binding sites within the LIF (stemness factor) prom

98 We provide evidence that ZEB1 binds not only to repress critical genes involving

99 The transcription factor ZEB1 binds preferentially to the nonrisk allele, leading

100 ators (p300) although conditions under which ZEB1 binds these cofactors are not elucidated.

101 e EMT, zinc finger E-box binding homeobox 1 (ZEB1) binds and silences IRF1.

102 Both TGF-beta- and MYC-induced EMT required ZEB1, but engaged distinct TGF-beta-dependent and vitami

103 s, through posttranscriptional regulation of ZEB1, but it also regulated the expression of numerous Z

104 etween the microRNA-200 (miR-200) family and ZEB1, but the precise mechanisms by which ZEB1-dependent

105 cogenic MUC1-C subunit induces expression of ZEB1 by a NF-kappaB (nuclear factor kappa B) p65-depende

106 ct activation of Ccr2 In turn, expression of ZEB1 by TAMs induced Ccl2, Cd74, and a mesenchymal/stem-

107 Functionally, we found that ZEB1 causally promotes malignant progression of HBECs an

108 pied by downregulation of either ZEB1 or the ZEB1 cofactor, BRG1.

109 nal regulatory networks and new factors (eg, ZEB1) controlling early stages of cardiomyocyte differen

110 a reciprocal feedback loop between GRHL2 and ZEB1 controls epithelial versus mesenchymal phenotypes a

111 Meta-analysis of ZEB1 copy number status in 2,988 cases of glioma reveale

112 also expressed in UM and high expression of ZEB1 correlates with UM advancement, but has little effe

113 observe that IRF1 expression is mediated by ZEB1 de-repression, and our study demonstrates how airwa

114 mes of over 4000 brain cancers we identified ZEB1 deletion in 15% (grade II and III) and 50% of glio

115 in 2,988 cases of glioma revealed disruptive ZEB1 deletions associated with decreased survival.

116 Additionally, ZEB1-dependent derepression of the miR-200 and miR-183 t

117 Zeb1-dependent EMT enhances tumor cell responsiveness to

118 nd ZEB1, but the precise mechanisms by which ZEB1-dependent EMT promotes malignancy remain largely un

119 tumor cell interactions regulated by miR-200/Zeb1-dependent EMT that activate intracellular signaling

120 lated the expression of E-cadherin and other ZEB1-dependent genes, through posttranscriptional regula

121 We found a similar ZEB1-dependent repression of EPCAM expression in human p

122 ponsible for the development of HCC-BDTT via ZEB1-directed EMT activation and Sec23a-mediated secreto

123 f these triplets in the homologous region of ZEB1 does not affect protein translation.

124 de evidence for two sequential inductions of ZEB1 during Ras transformation of MEFs.

125 us, we have identified a novel TXNIP/miR-200/Zeb1/E-cadherin signaling pathway that, for the first ti

126 ZEB1, encoding a transcription repressor essential for T

127 ulate each other's transcriptional activity: ZEB1 enhances TCF4/beta-catenin-mediated transcription a

128 ancer (CRC) cells with active Wnt signaling, ZEB1 enhances transcriptional activation of LAMC2 and uP

129 n become epithelioid but not vice versa; and ZEB1 exerts its tumorigenic effects by promoting cell de

130 Here we report that ZEB1 exerts the opposite effect in EGFR-mutated lung can

131 that FOXC2 regulates EMT, stem cell traits, ZEB1 expression and metastasis in a p38-dependent manner

132 al cells (HBECs) and determined that EMT and ZEB1 expression are early, critical events in lung cance

133 In addition, ZEB1 expression in early stage IB primary NSCLC correlat

134 Mechanistically, ZEB1 expression in HBECs directly repressed epithelial s

135 uorescence immunohistochemistry demonstrated ZEB1 expression in keratocyte nuclei.

136 Mechanistically, ZEB1 expression in TAMs induced their polarization towar

137 tant proteins and up-regulated TGF-beta2 and ZEB1 expression in type II cells.

138 Zeb1 expression is elevated in the Sonic Hedgehog (SHH)

139 We further show that ZEB1 expression is regulated by the NFkappaB transcripti

140 IFN-gamma treatment to GCSCs induced ZEB1 expression, attenuating LIF activities.

141 ctors attenuated PDGFA/PDGFRalpha-stimulated ZEB1 expression, cell migration and GSC proliferation.

142 Here we describe that TAMs require ZEB1 for their tumor-promoting and chemotherapy resistan

143 that the EMT transcription factors GRHL2 and ZEB1 form a double negative regulatory feedback loop in

144 ription and, in turn, Wnt signaling switches ZEB1 from a repressor into an activator.

145 our findings uncover a new pathway in which ZEB1 functions as a key regulator for PDGFRalpha-driven

146 way that increases c-myc protein to activate ZEB1 gene expression leading to the elevated CSC phenoty

147 nchymal phenotype, whereas knocking down the ZEB1 gene in mesenchymal cells induced an epithelial phe

148 he loss of chromosome 10p, which harbors the ZEB1 gene, was frequently detected in epithelial variant

149 ogether, our results suggest that a miR-200, ZEB1, GRHL2 gene regulatory network may drive sarcoma ce

150 f both phospho-PDGFRalpha (p-PDGFRalpha) and ZEB1 had significantly shorter overall survival compared

151 Aberrant expression of ZEB1 has been reported in a variety of human cancers, wh

152 gulators of E-cadherin expression, including ZEB1, HDAC1, and MMP14.

153 E-cadherin-high nonmigratory state toward a ZEB1-high invasive state.

154 e absence of such Rb1 repression Ras induces ZEB1 in cancer cells.

155 he functional relationship between GRHL2 and ZEB1 in EMT/MET and tumor biology.

156 on level of claudin-7 and those of SPRY2 and ZEB1 in human colon tumors.

157 However, a role for ZEB1 in macrophages and TAMs has not been studied.

158 to mutant Ras causes dominant repression of ZEB1 in primary cells, but loss of the Rb1 pathway is a

159 Importantly, ZEB1 in TAMs was a factor of poorer survival in human ov

160 ltration and CCR2 expression correlated with ZEB1 in tumor cells, where along with CCL2 and CD74 dete

161 These two roles for ZEB1 in tumour progression can be distinguished by their

162 Overexpression of ZEB1 in type II cells decreased DNA binding of endogenou

163 he mesoderm stage; E-box-binding homeobox 1 (ZEB1) in the module correlated with postcardiac mesoderm

164 of Gnrh that acts both directly and through Zeb1, in GnRH neurons.

165 ation of EMT transcription factors, Slug and ZEB1, in HCT116 human colon cancer cells.

166 hymal transition (EMT) transcription factor, ZEB1, in minute volumes of sample.

167 t states characterized by high expression of ZEB1, including epithelial-mesenchymal transition in epi

168 it also regulated the expression of numerous ZEB1-independent genes with functions predicted to contr

169 These findings indicate that ZEB1-induced EMT and associated molecular changes in ESR

170 biomarker for cell survival mediated through ZEB1-induced tumor progression pathways.

171 lusion, Galpha12 overexpressed in HCC causes ZEB1 induction by deregulating p53-responsive miRNAs, wh

172 miR-200a/b, -192 and -215 by Galpha12 caused ZEB1 induction.

173 Silencing the EMT transcription factor ZEB1 inhibited both EMT-associated TF expression and coa

174 Knockdown of ZEB1 inhibited PDGFA/PDGFRalpha-stimulated glioma EMT, t

175 ranule neuron progenitors (GNPs) reveal that Zeb1 inhibits polarization and retains progenitors in th

176 defective mucosal antiviral response through ZEB1-initiated epigenetic silencing.

177 Wnt signaling turns ZEB1 into an activator by replacing binding of CtBP/BRG1

178 The transcription factor ZEB1 is a known driver of EMT, and mediators of ZEB1 rep

179 We conclude that ZEB1 is a major oncogenic factor required for UM progres

180 ZEB1 is a prime element of a network of transcription fa

181 MT, invasiveness and growth, suggesting that ZEB1 is a promising therapeutic target for treating glio

182 ZEB1 is a zinc finger E-box binding transcription factor

183 ZEB1 is also a key determinant of cell plasticity, endow

184 ZEB1 is also expressed in UM and high expression of ZEB1

185 ZEB1 is best known for driving an epithelial-to-mesenchy

186 like properties following loss of UBQLN1 and ZEB1 is capable of repressing expression of UBQLN1, sugg

187 Although ZEB1 is classically linked to epithelial-mesenchymal tra

188 Beyond its well-documented role in EMT, ZEB1 is important for maintaining repression of cdki.

189 We further demonstrated that ZEB1 is required for early cardiomyocyte differentiation

190 Interestingly, we found that ZEB1 is required for induction of mesenchymal-like prope

191 ing protein GRB2 and an SH3-domain ligand in ZEB1 is required for SPRR2a-induced synergic suppression

192 Here we show that Ras induction of ZEB1 is required for tumour initiation in a lung cancer

193 A lower threshold of ZEB1 is sufficient for cancer initiation, whereas furthe

194 Indeed, heterozygous mutation of ZEB1 is sufficient for elevated cdki expression, leading

195 Ectopic ZEB1 is sufficient for IRF1 silencing, whereas ZEB1 knoc

196 ZEB1 is then further induced by Ras, beyond the level se

197 The Zinc-finger E-box-binding Homeobox-1 (ZEB1) is a transcription factor that promotes epithelial

198 ion of zinc finger E-box binding homeobox 1 (ZEB1) is associated with tumor grade and metastasis in l

199 e EMT program on its own, as orchestrated by Zeb1, is sufficient to incite metastatic outgrowth by ca

200 96 repressed common targets, including SLUG, ZEB1, ITGB1, and KLF4.

201 ducer ZEB1, as these effects are reversed by ZEB1 knock-down by means of RNA interference.

202 ZEB1 knockdown in GCSCs caused LIF induction commensurat

203 In addition, Zeb1 knockdown mimicked the miR-200 effects on beta cell

204 B1 is sufficient for IRF1 silencing, whereas ZEB1 knockdown partially restores IRF1-IFNL upregulation

205 We also identify the EMT-regulator ZEB1-known to directly repress E-cadherin/CDH1-as a down

206 duces the level of transcriptional repressor ZEB1, leading to induced expression of miR-183-5p.

207 activation and the transcriptional repressor ZEB1, leading to induction of miR-183-5p and down-regula

208 Because miR-200 represses Bmi1, induction of ZEB1 leads to induction of Bmi1.

209 ASF3 in breast cancer cells leads to reduced ZEB1 levels and increased miR-200 and E-cadherin levels,

210 A.X levels correlate inversely with Slug and ZEB1 levels.

211 Therefore, ZEB1 may play a role in both corneal stromal and endothe

212 UC1-C induces EMT and cellular invasion by a ZEB1-mediated mechanism.

213 -2 acts together with PI3K/AKT to regulate a ZEB1-miR-200 feedback loop in PDGFRalpha-driven gliomas.

214 es the opposing effects of mutant Ras on the ZEB1-miR-200 loop in primary versus cancer cells.

215 argeting AUF1, which binds the 3'-UTR of the ZEB1 mRNA and reduces its turnover.

216 In turn, ZEB1 associates with MUC1-C and the ZEB1/MUC1-C complex contributes to the transcriptional s

217 er than that of affected individuals without ZEB1 mutations (46.5 D; P = .004).

218 Affected individuals with ZEB1 mutations demonstrated a mean keratometric value of

219 affected individuals with PPCD secondary to ZEB1 mutations.

220 n NSCLC cells reduced a cohort of molecules (ZEB1, N-cadherin, Vimentin, and/or Snail1) critical for

221 Importantly, overexpression of ZEB1 or miR-200 antagonists in HFL type II cells also in

222 t is phenocopied by downregulation of either ZEB1 or the ZEB1 cofactor, BRG1.

223 n of key transcription factors (Snail, Slug, Zeb1) or by acquiring drug resistance produces a similar

224 lator, Zinc finger E-box binding homeobox 1 (ZEB1), or overexpression of the ZEB1-repressed microRNAs

225 athways (for example, Wnt, TGF-beta, mir200, ZEB1, OVOL2, p63 and p300) and translational implication

226 the nuclear factor-kappaB (NF-kappaB) p65-->ZEB1 pathway and confers a poor prognosis.

227 ects on beta cell apoptosis, suggesting that Zeb1 plays an important role in mediating miR-200 effect

228 We find that plastic non-CSCs maintain the ZEB1 promoter in a bivalent chromatin configuration, ena

229 MUC1-C occupies the ZEB1 promoter with NF-kappaB p65 and thereby promotes ZE

230 l dysfunction, these findings also show that ZEB1 promotes metastasis through a heretofore unapprecia

231 Thus, Zeb1 proteins employ several evolutionary conserved mech

232 redicted binding of the transcription factor ZEB1 rather to the nonrisk allele, which was confirmed e

233 Here, we show that TCF4 and ZEB1 reciprocally modulate each other's transcriptional

234 morigenesis, we found that downregulation of ZEB1 reduces the expression of LAMC2 in vivo.

235 1 is a known driver of EMT, and mediators of ZEB1 represent potential therapeutic targets for metasta

236 homeobox 1 (ZEB1), or overexpression of the ZEB1-repressed microRNAs (miRNAs), miR-200c, miR-183, mi

237 ine signaling stimulating VM is regulated by ZEB1-repressed miRNA clusters.

238 However, in CRC cells with inactive Wnt, ZEB1 represses both genes.

239 and gain of function analyses revealed that Zeb1 represses cdh1 expression to fine-tune adhesiveness

240 ZEB1 represses miR-200 in the context of a mutual repres

241 soforms is directly regulated by miR-200 and ZEB1, respectively, and their upregulation in metastatic

242 Knockdown of ZEB1 resulted in more profound reduction of nonrisk alle

243 ase in fluvastatin sensitivity; knocking out ZEB1 reversed this effect.

244 roRNAs (miR-200 family, miR-150) that target ZEB1 RNA.

245 ion of zinc finger E-box binding homeobox 1 (ZEB1) sensitized tumor cells to the antiproliferative ac

246 Together, these results indicate that ZEB1 sensitizes lung adenocarcinoma cells to metastasis

247 modulating CSC properties via CD117-mediated ZEB1 signaling pathway.

248 hat MUC1-C-induced activation of NF-kappaB-->ZEB1 signaling represses the TLR9 (toll-like receptor 9)

249 Knockdown of the EMT regulator ZEB1 significantly reduced leukemic blast invasion.

250 ZEB1 silences IRF1 through the catalytic activity of the

251 ous injection, a feature diminished by TF or ZEB1 silencing.

252 box-binding homeobox 1 transcription factor (ZEB1), siRNA-mediated knockdown and overexpression exper

253 pression of mesenchymal markers (CXCR4, VIM, ZEB1, SNAI2, and CDH2), compared with cells not exposed

254 n of the EMT-activating transcription factor ZEB1 stimulated Golgi compaction and relieved microRNA-m

255 leads to derepression of the miR-200 target ZEB1, stimulates the epithelial to mesenchymal transitio

256 th-inhibiting effect, EGFR inhibitor-induced ZEB1 strongly promotes EMT-dependent resistance to EGFR

257 nduction is required to reach a threshold of ZEB1 sufficient for repression of miR-200 and tumor inva

258 ranscriptional repression of this cluster by ZEB1, suggesting a reciprocal feedback loop.

259 unsuspected intrinsic oncogenic functions of ZEB1 that impact tumorigenesis from its earliest stages.

260 ated with the development of PPCD, including ZEB1 that is responsible for PPCD3.

261 eased the levels of OCT4 and its target gene ZEB1, thereby counteracting the increase of OCT4 induced

262 ulate expression of the transcription factor ZEB1, thereby linking tumor initiation to the subsequent

263 ce was directly mediated through SRC but not ZEB1; therefore, cotargeting EGFR and SRC synergisticall

264 ion of the epithelial-to-mesenchymal inducer ZEB1 through targeting AUF1, which binds the 3'-UTR of t

265 The ability of ZEB1 to activate/repress its target genes depends on its

266 CRIPTO1 activated SRC and ZEB1 to promote EMT via microRNA-205 (miR-205) downregul

267 t TGFbeta activates the transcription factor ZEB1 to repress Notch3, thereby limiting terminal differ

268 ll lines, mediated through direct binding of ZEB1 to the EPCAM promoter.

269 as also induces the EMT transcription factor ZEB1 to trigger tumor invasion and metastasis.

270 esses E-cadherin and miR-200, independent of Zeb1, to form a double-negative feedback loop.

271 coded by PTPN11) upregulates an EMT inducer, ZEB1, to mediate PDGFRalpha-driven glioma EMT, invasion

272 , GATA3, TCF7 (TCF-1), AHR, SOX4, RUNX2, and ZEB1 transcript levels are higher in CD56(bright) cells,

273 The ZEB1 transcription factor is best known as an inducer of

274 oter with NF-kappaB p65 and thereby promotes ZEB1 transcription.

275 s identify a mechanism through which Wnt and ZEB1 transcriptional activities are modulated, offering

276 loop between the microRNA-200 family and the Zeb1 transcriptional repressor is a master EMT regulator

277 T, but not cHCC, exhibited overexpression of ZEB1, Twist, transforming growth factor-beta receptor ty

278 cleotide changes within the coding region of ZEB1 underlie the pathogenesis of PPCD in 4 of 23 Czech

279 ZEB1 up-regulation is responsible for the MSX1-induced m

280 200c was found to be important in modulating ZEB1 upregulation by ERG.

281 Mechanistically, ZEB1 upregulation by SPRY2 results from the combined ind

282 l surface CDH1 and suppressed CDH3, VIM, and ZEB1 upregulation.

283 activity of statins, and induction of EMT by ZEB1 was sufficient to phenocopy the increase in fluvast

284 ollowing 2 novel frameshift mutations within ZEB1 were identified: c.2617dup in exon 8 in a 22-year-o

285 ctor zinc finger enhancer-binding protein 1 (ZEB1), which in turn is a direct target for repression b

286 anscription factors SNAI1, SNAI2, TWIST1 and ZEB1, which bind to E-box sites in the EpCAM promoter.

287 findings suggest that the miR-200 family and ZEB1, which exist in a double-negative feedback loop reg

288 of transcription factors SNAI1, TWIST1, and ZEB1, which regulate the epithelial-to-mesenchymal trans

289 A key Wnt target is the transcription factor ZEB1 whose expression by cancer cells promotes tumor inv

290 ed GRHL2 expression by direct interaction of ZEB1 with the GRHL2 promoter, inducing EMT.

291 lial-to-mesenchymal transition (EMT) markers ZEB1, ZEB2 and CDH2 (which encodes N-cadherin).

292 ted in Dicer-KO CDs, its direct target genes Zeb1, Zeb2, and Snail2 are upregulated, and miRNA-deplet

293 TGFbeta receptor TGFBR2 and the EMT inducers ZEB1, ZEB2, and the snail transcriptional repressor SNAI

294 ive major EMT regulatory genes (Snai1, Slug, Zeb1, Zeb2, and Twist1) involved in EMT.

295 tion through its impaired ability to inhibit ZEB1/ZEB2 and acquired concomitant ability to repress ne

296 mediated through the opposite regulation of ZEB1/ZEB2 and miR-200b and miR-200c.

297 otes the epithelial state by suppressing the Zeb1/Zeb2 epithelial gene transcriptional repressors.

298 0s regulate E-cadherin by directly targeting ZEB1/ZEB2, which are transcriptional repressors of E-cad

299 Mechanistically, we find that the ZEB1 (zinc finger E-box binding homeobox 1) transcriptio

300 we found that miR-200 targeted and decreased Zeb1 (zinc finger E-box-binding homeobox 1) and promoted