ライフサイエンスコーパス: ZEB1

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

2 ess, including the upregulation of SNAI1 and ZEB1.

3 leading to Notch1-dependent upregulation of Zeb1.

4 hymal/glycolytic shifts involving YKL-40 and ZEB1.

5 al polarity master genes via upregulation of ZEB1.

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

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

8 PDGFRbeta through the direct suppression of ZEB1.

9 also Src inhibition reduced the induction of ZEB1.

10 ssor of the established PPCD-associated gene ZEB1.

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

12 scription factors JUN and SP1 in addition to ZEB1.

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

14 11, CCR4, PLCG1, CDKN2A, ARID1A, RPS6KA1 and ZEB1.

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

16 , reciprocal regulation of EMT by UBQLN1 and ZEB1.

17 mparison of relative changes of Galpha12 and ZEB1.

18 metastatic disease due to high expression of ZEB1.

19 l marker E-cadherin with concomitant gain of ZEB1.

20 ion of its target genes, including Snai1 and ZEB1.

21 er region, and demonstrate LIF repression by ZEB1.

22 primarily via crosstalk with E-cadherin and ZEB1.

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

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

25 1, miR-200a, miR-200c, miR-429), which share Zeb1/2 as a common target mRNA, were upregulated togethe

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

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

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

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

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

31 ZEB1, a master epithelial-to-mesenchymal transition-indu

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

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

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

35 We derive a stroma-corrected ZEB1-activated transcriptional signature and demonstrate

36 ZEB1 and activated PDGFRalpha were coexpressed in invasi

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

38 erol relying on the increased recruitment of ZEB1 and CtBP complex to SREBF2 promoter.

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

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

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

42 multivariate survival analysis reveals that ZEB1 and its expression signature are significantly asso

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

44 Galpha12QL induced ZEB1 and other epithelial-mesenchymal transition markers

45 he protein levels of the mesenchymal markers ZEB1 and Snail.

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

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

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

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

50 reast cancer cells by forming a complex with ZEB1 and transcriptionally repressing SREBF2 expression.

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

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

53 ZEB1 and ZEB2 are zinc-finger E homeobox-binding transcr

54 sm distinct from its ability to downregulate Zeb1 and Zeb2 expression, because silencing them only ma

55 mesenchymal transition (EMT) by suppressing Zeb1 and Zeb2 expression.

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

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

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

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

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

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

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

63 Targeting MUC1-C, ZEB1, and DNMT3b thereby decreases methylation of the Cp

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

65 etastasis-associated markers VIMENTIN, SLUG, ZEB1, and MMP9, with a concurrent decrease in mRNA expre

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

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

68 ormed for vimentin, N-cadherin, ROCK1, RhoA, ZEB1, and Snail.

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

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

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

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

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

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

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

76 l mechanism of TMEJ regulation, highlighting ZEB1 as a key player in genome stability during cancer p

77 This work recognizes ZEB1 as a key regulator of cutaneous wound healing that

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

79 ploying YKL-40 as a resistance biomarker and ZEB1 as a target to prevent resistance could fulfill the

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

81 was used to elucidate the effect of elevated ZEB1, as noted during hyperglycemia.

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

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

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

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

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

87 Under different glycemic conditions, ZEB1 binding to E-cadherin promoter was investigated usi

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

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

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

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

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

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

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

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

96 by directly targeting EMT-promoting factors ZEB1, cdk6, and Snail.

97 We identify the NuRD complex as a ZEB1 co-repressor and the Rab22 GTPase-activating protei

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

99 In turn, MUC1-C/ZEB1 complexes recruit DNA methyltransferase 3b (DNMT3b)

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

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

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

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

104 Zeb1-deficient injured muscles also display a delayed an

105 Compared to wild-type counterparts, Zeb1-deficient injured muscles exhibit enhanced damage t

106 Macrophages in Zeb1-deficient injured muscles show lower phosphorylatio

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

108 ZEB1 deletion in stromal fibroblasts increases acetylati

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

110 Zeb1-dependent EMT enhances tumor cell responsiveness to

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

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

113 rsible; rather ERK1/2 hyperactivation drives ZEB1-dependent epithelial-to-mesenchymal transition and

114 Here, we show that Zeb1 depletion suppresses stemness, colonization and the

115 In conclusion, we showed that ZEB1 directly inhibits the expression of POLQ and, there

116 Depletion of Zeb1 disrupts this positive feedback loop in the tumor p

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

118 ZEB1, encoding a transcription repressor essential for T

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

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

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

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

123 ecific relationship between stroma-corrected ZEB1 expression and decreased immune activity in multipl

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

125 a novel association between stroma-adjusted ZEB1 expression and tumor immune activity and addresses

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

127 n state where ZEB2 expression is replaced by ZEB1 expression associated with gain of an invasive phen

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

129 Mechanistically, ZEB1 expression in HBECs directly repressed epithelial s

130 Mechanistically, ZEB1 expression in TAMs induced their polarization towar

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

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

133 Consequently, ZEB1 expression prevented TMEJ activity, with a major im

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

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

136 icroenvironment (TME) contribute to aberrant Zeb1 expression.

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

138 Moreover, downregulation of POLQ by ZEB1 fostered micronuclei formation in TNBC tumor cell l

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

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

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

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

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

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

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

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

147 Zinc finger E-box binding homeobox 1 (Zeb1) has been demonstrated to participate in the acquis

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

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

150 udin-low tumor cells or forced expression of ZEB1 in basal-like tumor cells, two triple-negative brea

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

152 The role of ZEB1 in cutaneous wounds was assessed using Zeb1(+/-) mi

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

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

155 EGFR or ERBB2 upregulated ZEB1 in nonadherent cells, which caused resistance to ce

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

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

158 as weakened activity against its target gene ZEB1 in thyroid cancer cells, likely explaining the redu

159 In turn, ectopic Zeb1 in tumor cells increases VEGFA production and recip

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

161 However, the role of stromal ZEB1 in tumour progression remains unexplored.

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

163 of the zinc finger E-box binding homeobox 1 (ZEB1) in claudin-low tumor cells or forced expression of

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

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

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

167 glycoprotein YKL-40 and transcription factor ZEB1, in later clones, implicating these changes as trea

168 a mouse model of breast cancer, we show that ZEB1 inactivation in stromal fibroblasts suppresses tumo

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

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

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 an Epigenome shRNA dropout screen, to define ZEB1 interactors that are critical to metastatic NSCLC.

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

179 We found that ZEB1 is a critical EMT factor for mutant beta-catenin-me

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

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

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

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

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

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

186 ZEB1 is also known to contribute to endothelial cell sur

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

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

189 es that the zinc-finger transcription factor ZEB1 is predominantly expressed in the stroma of several

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

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

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

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

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

195 ZEB1 is upregulated in the undamaged and regenerating my

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

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

198 hieved by constitutive ectopic expression of Zeb1, is sufficient to drive cells out of the E/M hybrid

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

200 We studied transcriptional regulation of ZEB1, ITGA3, ITGB1, JNK, and ENT1 by ZIP4 using chromati

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 B(+/-) as well as in db/db mice subjected to ZEB1 knockdown.

206 ZEB1-knockdown cells had increased sensitivity to gemcit

207 es, and in pancreatic cells from KPC and KPC-ZEB1-knockout mice, and pancreatic spheroids were establ

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

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

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

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

212 al of breast cancer patients expressing high ZEB1 levels in the stroma.

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

214 Under hyperglycemic conditions, ZEB1 lost its ability to bind E-cadherin promoter.

215 Zeb1(+/-) mice exhibited compromised wound closure compl

216 ZEB1 in cutaneous wounds was assessed using Zeb1(+/-) mice, as Zeb1(-/-) mice are not viable.

217 wounds was assessed using Zeb1(+/-) mice, as Zeb1(-/-) mice are not viable.

218 -2 acts together with PI3K/AKT to regulate a ZEB1-miR-200 feedback loop in PDGFRalpha-driven gliomas.

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

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

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

222 Rab22 GTPase-activating protein TBC1D2b as a ZEB1/NuRD complex target.

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

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

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

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

227 The dominant proteins downregulated after ZEB1 overexpression functionally represented adherens ju

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

229 Our findings identify the ZEB1/p53 axis as a stroma-specific signaling pathway tha

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

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

232 AM, GPC1, WNT-2, EphA2, S100A4, PSCA, MUC13, ZEB1, PLEC1, HOOK1, PTPN6, and FBN1) in EV from patient-

233 Zinc finger E-box binding homeobox 1 (ZEB1), primarily studied in the context of tumor biology

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

235 These data indicate that ZEB1 protects muscle from damage and is required for its

236 IX and zinc finger E-box binding homeobox 1 (Zeb1) protein levels increased in 1% oxygen.

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

238 uggest that reversible switching of the ZEB2/ZEB1 ratio enhances melanoma metastatic dissemination.

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

240 Targeting ZEB1 reduces bevacizumab-resistant GBM phenotypes.

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

242 Here we report an unexpected role for ZEB1 regulating inflammatory and repair responses in dys

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

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

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

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

247 cancer (TNBC) subtypes, to demonstrate that ZEB1 represses POLQ expression.

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

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

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

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

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

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

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

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

256 ZEB1 silences IRF1 through the catalytic activity of the

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

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

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

260 ve for alpha-SMA, vimentin, CK7, N-cadherin, ZEB1, Snail, ROCK1, and RhoA.

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

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

263 Importantly, p53 ablation in ZEB1 stroma-deleted mammary tumours sufficiently recover

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

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

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

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

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

269 MuSCs require ZEB1 to maintain their quiescence, prevent their prematu

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

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

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

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

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

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

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

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

278 s the RASSF1A promoter in a complex with the ZEB1 transcriptional repressor.

279 directly and negatively regulates Snai1 and ZEB1, two zinc finger transcription factors that lead to

280 Of the EMT-associated transcription factors, ZEB1 uniquely promotes NSCLC disease progression.

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

282 200c was found to be important in modulating ZEB1 upregulation by ERG.

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

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

285 ht that targeting the angiocrine Jag1-Notch1-Zeb1-VEGFA loop decreases breast cancer aggressiveness a

286 vasion, mesenchymal markers (through the ERK-ZEB1-vimentin axis under certain conditions) and in vivo

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

288 eases expression of the transcription factor ZEB1, which activates expression of ITGA3 and ITGB1.

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

290 FOXM1 also upregulated ZEB1, which could act as a feedback inhibitor of FOXM1,

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

292 P4 to activate STAT3 to induce expression of ZEB1, which induced expression of ITGA3 and ITGB1 in KPC

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

294 CRISPR and pharmacologic targeting of ZEB1 with honokiol reversed the mesenchymal gene express

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

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

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

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

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

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