ライフサイエンスコーパス: slug

1 E-cadherin subsequent to decreased levels of SLUG.

2 ent upregulation of the transcription factor SLUG.

3 on of the proapoptotic gene, Puma (Bbc3), by Slug.

4 brogating the expression of the EMT mediator SLUG.

5 ng the expression of the zinc-finger protein SLUG.

6 r 1 (VEGFR1) and ligand D (VEGFD), SNAIL and SLUG.

7 ing pathways and the expression of Snail and Slug.

8 on of E-cadherin and decreased expression of Slug.

9 h levels of the metastasis regulator protein SLUG.

10 eased expression of the transcription factor Slug.

11 , SM22alpha, calponin, phospho-vimentin, and Slug.

12 or-promoting transcription factors, Sox9 and Slug.

13 e expression of the EMT transcription factor slug.

14 how that SOX2 is a transcriptional target of SLUG.

15 sed by joint knockdown of BMPR2 and HMGA1 or Slug.

16 ll as expression of the transcription factor Slug.

17 mesenchymal transition regulators: snail and slug.

18 tic activity in kleptoplasts retained by sea slugs.

19 euopisthobranch and panpulmonate snails and slugs.

20 In contrast, nonphosphorylatable Slug-4SA is not degraded by CHIP.

21 ssing the expression of transcription factor Slug, a key regulator of EMT.

22 illin affects the expression and activity of Slug, a key transcriptional regulator of EMT.

23 expansion, clonogenicity, and expression of Slug, a master regulator of MaSCs.

24 alphavbeta3 was necessary and sufficient for Slug activation, tumorsphere formation, and tumor initia

25 TGF-beta treatment enhanced Slug activity and thus increased miR-221 level in MCF-7

26 However, the means by which Slug activity is controlled remain unclear.

27 l Wnt/GSK3beta/beta-Trcp1 axis that controls Slug activity.

28 coy that competes with the E2-box binding of SLUG also increased the levels of plakoglobin mRNA, prot

29 leura is a diverse monophyletic clade of sea slugs among which only a small percentage of species can

30 ed the expression of the mesenchymal markers SLUG and ARF6.

31 the expression of the EMT program components Slug and Axl.

32 TGF-beta1-induced up-regulation of Snail and Slug and down-regulation of VE-cadherin.

33 Comparisons of endogenous Slug and E-cadherin expression in cultured normal human

34 Levels of slug and fascin correlated in PDAC cells; slug was found

35 EMT and mesenchymal differentiation through Slug and functions in tumor-suppressive programs by regu

36 We found that PBT-1 reduced the level of Slug and inhibits the migration, invasion, and filopodia

37 ctin-bundling protein fascin is regulated by slug and involved in late-stage PanIN and PDAC formation

38 Thus, transgenic mice expressing Slug and Kras in acinar cells were generated.

39 Thus, SLUG and miR-1/miR-200 act in a self-reinforcing regulat

40 s a clear relationship between expression of Slug and MITF, a transcription factor known to regulate

41 Consonant with these findings, nuclear Slug and Snail expression are increased in association w

42 tly greater expression of Ki67, p53, VEGFR1, SLUG and SNAIL in the metastases compared with the prima

43 luminal layer exploit the paralogous EMT-TFs Slug and Snail, respectively, which induce distinct EMT

44 GFR1, and FGFR2 as well as mesenchymal genes SLUG and SNAIL.

45 Slug and Sox9 induce MaSCs by activating distinct autore

46 Correlation between SLUG and SOX9 levels was observed remarkably, we therefo

47 We also show that coexpression of Slug and Sox9 promotes the tumorigenic and metastasis-se

48 versely, transient coexpression of exogenous Slug and Sox9 suffices to convert differentiated luminal

49 We have identified two TFs, Slug and Sox9, that act cooperatively to determine the m

50 residue thus leading to the upregulation of Slug and tumor progression.

51 on of E-cadherin and increased expression of Slug and vimentin, a mesenchymal marker.

52 panel, H2A.X levels correlate inversely with Slug and ZEB1 levels.

53 ctivated Notch-induced transcription factors Slug and ZEB1, and canonical Notch signaling was require

54 ing activation of EMT transcription factors, Slug and ZEB1, in HCT116 human colon cancer cells.

55 ly reverses these changes, as does silencing Slug and ZEB1.

56 in 3D growth, accompanied by upregulation of SLUG and ZEB2 and increased invasive properties.

57 We identified Slug and ZEB2 as direct functional targets of miR-218.

58 o cisplatin treatment through suppression of Slug and ZEB2.

59 ription factors, TWIST1, SNAI1/Snail1, SNAI2/Slug and ZEB2/Sip1, and are highly invasive.

60 rying or agriculturally important snails and slugs and as a paradigm group for the study of the evolu

61 s include migration vectors (such as snails, slugs and isopods) and pathogens (such as microsporidia,

62 chatinoid clades of the Stylommatophora (and slugs and shelled slugs), which diverged 90-130 MYA.

63 ct and systemic molluscicide for controlling slugs and snails in a wide range of agricultural and hor

64 egates, which first transform into migrating slugs and then into sessile fruiting structures.

65 cterial isolates acquired from a sponge, sea slug, and coral to examine the functional landscape of t

66 ibiting N-cadherin and transcription factors Slug, and pluripotency maintaining factors Nanog, c-Myc,

67 mal transition (EMT) genes including TWIST1, SLUG, and SNAIL.

68 ion of miR-34a and its direct targets Notch, Slug, and Snail.

69 anscription factors, Kruppel-like factor 15, Slug, and SPDEF, stimulated the herpes simplex virus typ

70 rotein expression levels of vimentin, snail, slug, and twist and a loss of the epithelial cell marker

71 In addition, we found that Snail-1, Slug, and Twist, all of which are known to act as EMT in

72 initiates antitumor activities by affecting Slug- and AKT-mediated metastasis and tumorigenesis.

73 echanically isolated from the CNS of the sea slug Aplysia californica, a well characterized neurobiol

74 to overcome these limitations using the sea slug Aplysia californica.

75 nes in the central nervous system of the sea slug Aplysia californica.

76 5-500 mum in diameter) isolated from the sea slug (Aplysia californica) central and rat (Rattus norve

77 adherin transcriptional repressors Snail and Slug are not implicated.

78 Some sea slugs are capable of retaining functional sequestered ch

79 Snail1 (Snail) and Snail2 (Slug) are transcription factors that share a similar DNA

80 erative and invasive properties, implicating Slug as a critical driver of disease progression.

81 of prostate adenocarcinoma, and we identify Slug as one of the phylogenetically conserved targets of

82 et (BRCA1), further studies demonstrate that Slug-as well as Snail-directly represses BRCA1 expressio

83 Surprisingly, Slug attenuated Kras-induced ADM development, ERK1/2 pho

84 In addition, Slug attenuated TGF-alpha-induced acinar cell metaplasia

85 Interestingly, depletion of Snail, but not Slug, attenuated TGF-beta1-induced down-regulation of VE

86 t cancer through the estrogen receptor alpha/Slug axis and that it is a potential noninvasive biomark

87 nducible factor 1alpha (Hif-1alpha), Snail1, Slug, basic fibroblast growth factor (bFgf), and retinal

88 Our data show that the Slug/beta-catenin-dependent activation of DNA damage sig

89 SLUG, beyond its known function as an epithelial-mesench

90 ver, miR-221 was specifically upregulated by Slug but not Snail.

91 lated E-cadherin, beta-catenin, vimentin and Slug, but it partially rescued Twist1-silenced ERalpha a

92 ncreased expression of a known EMT regulator Slug, but not TWIST or Snail.

93 MAR1-dependent transcriptional repression of Slug by direct recruitment of SMAR1/HDAC1 complex to the

94 f ductal markers and reversed the effects of Slug by inducing ductal structures.

95 oRNA screen revealed that ANGPTL1 suppressed SLUG by inducing expression of miR-630 in an integrin al

96 Overexpression of SLUG in the SLUG-deficient cancer cells significantly decreased the

97 Overexpression of SLUG in the SLUG-deficient cells elevated the motility of these cell

98 ctin promote lung metastasis by upregulating Slug, defining a mechanism through which cancer cells ca

99 VEGFA stimulates Sox2- and Slug-dependent cell invasion.

100 depletion of Klf4 was sufficient to initiate SLUG-dependent EMT.

101 We show here that either treatment blocked Slug-dependent repression of the E-cadherin promoter and

102 The ensuing Slug-dependent serine 139 phosphorylation of the DNA dam

103 ies support the concept that targeting Snail/Slug-dependent transcription repression complexes may le

104 onstrated by the inhibition of EMT following Slug depletion.

105 pment stages of D. discoideum when migrating slugs differentiate into fruiting bodies that contain pe

106 ymal markers and were phenocopied by LSD1 or Slug downregulation.

107 ylase 1 (HDAC1) recruitment and antagonizing Slug E-box binding.

108 nthophyll cycle were investigated in the sea slugs Elysia viridis and E. chlorotica using chlorophyll

109 Similarly, restoring paracrine TGF-beta-Slug-EMT signaling reactivated the transdifferentiation

110 We identify two proteins, SLUG (encoded by SNAI2 gene) and SOX9, which are associa

111 vivo analyses provided strong evidence that Slug enhances both tumor growth and metastatic phenotype

112 e and others previously established that the Slug epithelial-to-mesenchymal transition-inducing trans

113 Vimentin, ERK, and Slug exhibited overlapping subcellular localization in c

114 over, in contrast to Snail-expressing cells, Slug-expressing cells did not demonstrate increased coll

115 ased MT1-MMP expression and ERK1/2 activity, Slug-expressing cells failed to scatter in three-dimensi

116 scattering in three-dimensional collagen of Slug-expressing cells following ROCK1/2 inhibition was d

117 OCK1/2 increased migration and scattering of Slug-expressing cells in three-dimensional collagen and

118 inhibited bone marrow homing/engraftment of Slug-expressing K562 cells.

119 In addition, blocking ROCK1/2 activity in Slug-expressing Kras mice reversed the inhibitory effect

120 SLUG expression and binding are necessary for SOX9 promo

121 RasN17), significantly inhibited RCP-induced Slug expression and cancer cell invasion.

122 We then investigated how HER2 induced Slug expression and found, for the first time, that ther

123 ockdown of HSF-1 expression by siRNA reduced Slug expression and HRG-induced EMT.

124 some number control, spindle pole formation, Slug expression and satellite RNA suppression.

125 1 integrin efficiently inhibited RCP-induced Slug expression and subsequent cancer cell invasion.

126 31 cells impaired the induction of Snail and Slug expression by EGF, and this effect was associated w

127 TF, a transcription factor known to regulate Slug expression during development.

128 Taken together, our findings suggest that Slug expression during melanomagenesis is highest early

129 ys demonstrated decreased KLF4 and increased SLUG expression in advanced-stage primary prostate cance

130 omoter independent of heat shock, leading to Slug expression in breast cancer cells.

131 Moreover, Slug expression in melanomas was not associated with dec

132 A1, are direct transcriptional inhibitors of SLUG expression in mouse and human prostate cancer cells

133 we provide evidence that hTERT links Src to Slug expression in NE-induced ovarian cancer EMT and met

134 est early in the process and that persistent Slug expression is not required for melanoma progression

135 In addition, silencing of Slug expression significantly inhibited NE- and hTERT-in

136 s of melanoma arrays, however, revealed that Slug expression was actually higher in nevi than in prim

137 Notably, in an orthotopic tumor model, Slug expression was sufficient to induce collective inva

138 ional links between canonical Wnt signaling, Slug expression, EMT, and BRCA1 regulation.

139 s where its expression level correlates with Slug expression, enhanced invasiveness, and poor clinica

140 ockdown reduced the ability of Akt to induce Slug expression, indicating an essential role that HSF-1

141 s prevented HRG-induced HSF-1 activation and Slug expression.

142 nRNP A2/B1 reduced the activation of AKT and Slug expression.

143 elated with fibronectin matrix formation and Slug expression.

144 s/NF-kappaB signaling cascade and subsequent Slug expression.

145 n of beta1 integrin was sufficient to induce Slug expression.

146 Ectopic expression of RCP induced Slug expression.

147 nduced ovarian cancer cell invasion, EMT and Slug expression.

148 active Akt induced HSF-1 phosphorylation and Slug expression.

149 GSK3beta-mediated phosphorylation of Slug facilitates Slug protein turnover.

150 he development of a single-step method using slug-flow microextraction and nano-electrospray ionizati

151 gas-driven oscillatory motion of a biphasic slug for high-throughput in situ measurement and screeni

152 Blocking of SLUG function with a double-stranded DNA decoy that comp

153 nce 1 (GFI1) is comprised of conserved Snail/Slug/Gfi1 (SNAG) and zinc finger motifs separated by a l

154 This finding is significant because SLUG has been implicated in breast CSCs and TNBC.

155 On the contrary, knockdown of SLUG in SLUG-high cancer cells elevated the levels of plakoglobi

156 Forced expression of plakoglobin in SLUG-high cells had the reverse effects on cellular moti

157 mRNA, protein, and promoter activity in the SLUG-high triple negative breast cancer cells.

158 directly binds to the DNA-binding domain of Slug, impeding histone deacetylase 1 (HDAC1) recruitment

159 ranscription factor -2 ( SNAI2) (also called SLUG), implicating LGR4 in regulation of epithelial-mese

160 ts increase our understanding of the role of Slug in ADM, an early event that can eventually lead to

161 This study demonstrates a pivotal role for Slug in carcinoma cell survival, implying that disruptio

162 1b expression highly correlated with that of Slug in clinical samples of advanced disease.

163 ry stem cells, and that forced expression of Slug in collaboration with Sox9 in breast cancer cells c

164 e critical EndMT transcription factors Snail/Slug in involuting hemangiomas.

165 Expression of exogenous Slug in melanocytes and melanoma cells in vitro, however

166 The precise role of Slug in melanomagenesis remains to be elucidated and may

167 9 level is associated with the expression of Slug in non-small cell lung cancer.

168 On the contrary, knockdown of SLUG in SLUG-high cancer cells elevated the levels of pl

169 A role for Slug in the EMT-like loss of cell adhesion and increased

170 Overexpression of SLUG in the SLUG-deficient cancer cells significantly de

171 Overexpression of SLUG in the SLUG-deficient cells elevated the motility o

172 s directly correlated with the levels of the SLUG in these cells.

173 ntified the zinc-finger transcription factor Slug in WNK1-mediated control of endothelial functions.

174 inc finger transcriptional repressor protein Slug, in vimentin-deficient (VIM(-/-)) wounds.

175 Although Slug increased MT1-MMP expression and ERK1/2 activity, S

176 d that the transcriptional repressor protein SLUG increases the motility of the aggressive breast can

177 dherin transcriptional repressors, snail and slug, induced by transforming growth factor-beta1 or ext

178 This study thus implicates SLUG-induced repression of plakoglobin as a motility det

179 vation of a signaling cascade culminating in Slug induction, epithelial-to-mesenchymal transition and

180 -stimulated KLF4 degradation is required for SLUG induction.

181 Depletion of Slug inhibited EMT during tumorigenesis, whereas forced

182 In support of this idea, Slug inhibition by shRNA sensitized tumor cells to apopt

183 We found that SLUG inhibits the expression of plakoglobin gene directl

184 SLUG interacts directly with SOX9 and prevents it from u

185 We demonstrate that SLUG is a direct repressor of miR-1 and miR-200 transcri

186 Here we show that SLUG is a major regulator of mesenchymal differentiation

187 ictyostelium discoideum into a multicellular slug is known to result from single-cell chemotaxis towa

188 In the absence of Wnt signaling, Slug is phosphorylated by GSK3beta and subsequently unde

189 factor beta (TGFbeta)-induced prostatic EMT, SLUG is the dominant regulator of EMT initiation in vitr

190 Consistent with a role in metastasis, Slug knockdown in carcinoma cells suppressed lung coloni

191 onfirmed in human breast cancer cells, where Slug knockdown increased Puma expression and inhibited l

192 s, inhibition of Puma by RNA interference in Slug-knockdown cells rescued lung colonization, whereas

193 linositol 3'-kinase)/Akt phosphorylation and Slug level.

194 K3beta kinase activity is inhibited, nuclear Slug levels increase, and EMT programs are initiated.

195 ast cancers between Wnt signaling, increased Slug levels, and reduced expression of the tumor suppres

196 Attempts to group these slug-like taxa into a single 'halwaxiid' clade neverthel

197 We assessed whether blocking Snail/Slug-LSD1 interaction by treatment with Parnate, an enzy

198 exhibited nuclear localization of Twist and Slug, markers of epithelial-mesenchymal transition (EMT)

199 The accumulation of nondegradable Slug may further lead to the repression of E-cadherin ex

200 a repressor in controlling HIF-1alpha/HDAC1/Slug-mediated cancer cell invasion and is a potential th

201 rast, SOX9 bound the SLUG promoter to induce SLUG-mediated cell invasion with a spindle-like phenotyp

202 downregulated during tumorigenesis via Snail/Slug-mediated E-cadherin transcriptional reduction.

203 herin and occludin expression and suppresses Slug-mediated epithelial-mesenchymal transition (EMT) an

204 Daxx also suppresses Slug-mediated lung cancer metastasis in an orthotopic lu

205 er cells results in a coordinative action of Slug-mediated repression of E-cadherin transcription, as

206 of the DgcA gene blocked the transition from slug migration to fructification and the expression of s

207 ive (GABA-ir) neurons in four species of sea slugs (Mollusca, Gastropoda, Opisthobranchia, Nudibranch

208 discovered that IMP3 binds avidly to SNAI2 (SLUG) mRNA and regulates its expression by binding to th

209 on and elevated the levels of VIM, ZEB1, and SLUG mRNAs.

210 y regulated the expression of EndMT markers (Slug, N-cadherin, alpha-SMA) in EC exposed to low shear

211 2) induced alphavbeta3 expression, enhancing Slug nuclear accumulation and MaSC clonogenicity.

212 Kras mice reversed the inhibitory effects of Slug on ADM, ERK1/2 phosphorylation, proliferation and f

213 lated by the usual increase in expression of Slug or Snail, the transcriptional regulators for E-cadh

214 Inhibition of either Slug or Sox9 blocks MaSC activity in primary mammary epi

215 Inhibition of either SLUG or SOX9 sufficiently inhibits CSCs in human lung ca

216 id to divide the reagent phase into discrete slugs or droplets.

217 ic expression of hTERT induced expression of Slug, ovarian cancer cell epithelial-mesenchymal transit

218 mples, we confirmed that the HIF-1alpha/Daxx/Slug pathway is an outcome predictor.

219 provide evidence of a de novo GSK3beta-CHIP-Slug pathway that may be involved in the progression of

220 ciated MaSCs require a TGF-beta2/alphavbeta3/Slug pathway, which may contribute to breast cancer prog

221 invasion by inhibiting the HIF-1alpha/HDAC1/Slug pathway.

222 hat the convergence of the cyclin D1b/AR and Slug pathways results in the activation of processes cri

223 ome-team offensive performance, for example, slugging percentage, but did not similarly affect away-t

224 scaffold to recruit Slug to ERK and promote Slug phosphorylation at serine-87.

225 s established a requirement for ERK-mediated Slug phosphorylation in EMT initiation.

226 In one such system, the predatory sea slug Pleurobranchaea, appetite is readily quantified in

227 herin is post-transcriptionally regulated by Slug-promoted miR-221, which serves as an additional blo

228 HSF-1 bound to and transactivated the Slug promoter independent of heat shock, leading to Slug

229 matrix attachment region site present in the Slug promoter restores E-cadherin expression, SMAR1 also

230 In contrast, SOX9 bound the SLUG promoter to induce SLUG-mediated cell invasion with

231 ranscriptional corepressor and ligand of the Slug promoter, ZBRK1.

232 heat shock factor-1 (HSF-1), located in the Slug promoter.

233 T1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes.

234 mediated phosphorylation of Slug facilitates Slug protein turnover.

235 arian cancer aggressiveness through inducing Slug, providing novel biomarkers and potential therapeut

236 Consistent with a pivotal role for a Slug-Puma axis in metastasis, inhibition of Puma by RNA

237 ll survival, implying that disruption of the Slug-Puma axis may impinge on the survival of metastatic

238 The survival function of the Slug-Puma axis was confirmed in human breast cancer cell

239 xpression of mesenchymal proteins (VIMENTIN, SLUG), reduced migration and tumor sphere formation, and

240 finger-containing transcriptional repressor, Slug, represses E-cadherin transcription and enhances ep

241 trolling fibroblast proliferation, TGF-beta1-Slug signaling, collagen accumulation, and EMT processin

242 uppression of MARCKS phosphorylation and AKT/Slug signalling pathway but not the expression of total

243 In this study, we examine the role of Slug (Snai2) in regulating pancreatic cancer cell scatte

244 t, the contribution of Snail-related protein Slug (Snai2) to ADM development is not known.

245 del that N-cadherin (Cdh2) expression causes Slug (Snai2) upregulation, which in turn promotes carcin

246 Slug (Snai2), a member of the Snail family of zinc finge

247 EMT master regulator Snail (SNAI1), but not Slug (SNAI2), shows evidence of Pol II pausing before ac

248 at regulates the transcriptional activity of Slug (SNAI2).

249 repressors, which include Snail (SNAIL1) and Slug (SNAI2).

250 expression in sh-AhR cells reduced Snail and Slug/Snai2 levels and cell migration and restored E-cadh

251 on of the EMT-promoting transcription factor SLUG/SNAI2, repressing its transcription by recruiting H

252 sed expression of mesenchymal markers Snail, Slug/Snai2, vimentin, fibronectin, and alpha-smooth musc

253 nd a basal phenotype (SMO (smoothened), p63, SLUG (snail-2), KER14 (keratin-14) and VIM (vimentin)).

254 rkers and transcription factors (N-cadherin, Slug, Snail and Zeb1), and upregulation of E-cadherin.

255 E-cadherin, and decreased those of vimentin, Slug, Snail, matrix metalloproteinase (MMP)-2, -9, and a

256 TS subpopulation expresses higher levels of SLUG, SNAIL, VIMENTIN and N-CADHERIN while show a lack o

257 Slug (Snail2) plays critical roles in regulating the epi

258 stic insight into the regulation of CSCs via SLUG-SOX9 regulatory axis, which represents a potential

259 ir) neurons in the buccal ganglia of six sea slug species (Mollusca, Gastropoda, Euthyneura, Nudipleu

260 that Sentinel (S) cells of the multicellular slug stage of the social amoeba Dictyostelium discoideum

261 PLZF or Slug stimulated productive infection 20- or 5-fold, resp

262 e infection 20- or 5-fold, respectively, and Slug stimulated the late glycoprotein C promoter more th

263 a3, Src kinase, and the transcription factor Slug suppresses PUMA in these cells, promoting tumor ste

264 peptide corresponding to the SNAG domain of Slug, suppresses the motility and invasiveness of cancer

265 ased expression of E-cadherin, the canonical Slug target in EMT.

266 s and an unanticipated link between WNK1 and Slug that is important for angiogenesis.

267 uces the EMT-regulating transcription factor Slug that marks epithelial transdifferentiation into M c

268 TP-dependent manner and was expressed at the slug tip, which is the site of stalk cell differentiatio

269 to the E-box used by the suppressor protein Slug to block OCLN expression.

270 ent, vimentin acted as a scaffold to recruit Slug to ERK and promote Slug phosphorylation at serine-8

271 perates with the transcription factor Snail2/Slug to modulate neural crest development in Xenopus.

272 a pivotal step in controlling the ability of Slug to organize hallmarks of EMT.

273 ormation were restored by exposing DgcA-null slugs to wild-type secretion products or to c-di-GMP.

274 1ph and epigenetic reprogramming to suppress Slug transcription to inhibit EMT.

275 Mutation of the putative HSEs ablated Slug transcriptional activation induced by HRG or HSF-1

276 eness by inhibiting expression of the SNAI2 (Slug) transcriptional repressor, which leads to expressi

277 rred in the absence of induction of SNAIL or SLUG, two canonical inducers of EMT in many other settin

278 IP stabilizes the wtSlug protein and reduces Slug ubiquitylation and degradation.

279 to form multicellular aggregates observed as slugs under starvation conditions.

280 our results provide the first evidence that Slug-upregulated miR-221 promotes breast cancer progress

281 novel Akt-HSF-1 signaling axis that leads to Slug upregulation and EMT, and potentially contributes t

282 genitor like properties, involving Snail and Slug upregulation, mammosphere formation and aldehyde de

283 ll expansion, together with miR-452 loss and Slug upregulation, providing a novel mechanism whereby c

284 sential role that HSF-1 plays in Akt-induced Slug upregulation.

285 The positive association between HSF-1 and Slug was confirmed by immunohistochemical staining of a

286 Slug was dramatically upregulated in metastases relative

287 The prosurvival effect of Slug was found to be caused by direct repression of the

288 of slug and fascin correlated in PDAC cells; slug was found to regulate transcription of Fascin along

289 ned that transcriptional induction of SNAI2 (Slug) was essential for cyclin D1b-mediated proliferativ

290 romyelocytic leukemia zinc finger (PLZF) and Slug were induced more than 15-fold 3 h after DEX treatm

291 f the Stylommatophora (and slugs and shelled slugs), which diverged 90-130 MYA.

292 ced upregulation of the transcription factor Slug, which mediates epithelial-mesenchymal transition a

293 Co-expression of Slug with Kras also attenuated chronic pancreatitis-indu

294 ting protein (CHIP) interacts with wild-type Slug (wtSlug).

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

296 ression of key transcription factors (Snail, Slug, Zeb1) or by acquiring drug resistance produces a s

297 d miR-96 repressed common targets, including SLUG, ZEB1, ITGB1, and KLF4.

298 are five major EMT regulatory genes (Snai1, Slug, Zeb1, Zeb2, and Twist1) involved in EMT.

299 ons were observed between miR-218 levels and Slug/ZEB2 levels in cancer tissue samples.

300 asis of lung cancer in part by modulation of Slug/ZEB2 signaling, and provide a potential therapeutic