ライフサイエンスコーパス: EMT

1 EMT (epithelial-mesenchymal-transition)-signaling regula

2 EMT-like and EMT-independent amoeboid cell subsets showe

3 Information about EMT may also inform other phase transitions in cancer, s

4 s were incapable of spontaneously activating EMT, whereas the others contained large populations of E

5 DNM3OS knockdown results in altered EMT-linked genes/pathways, mesenchymal-to-epithelial tra

6 transition (EMT), we investigated ZIP6 in an EMT paradigm using ZIP6 knockout cells, mass spectrometr

7 ls, but rather TGFbeta-inhibition induced an EMT-intermediate.

8 revealed that PHF8 overexpression induces an EMT-like process, including the upregulation of SNAI1 an

9 te that hnRNPF negatively correlates with an EMT gene signature and positively correlates with patien

10 totoxicity), proliferation (EGF + FGF-2) and EMT (TGF-beta1).

11 a common endpoint of both EMT-dependent and EMT-independent cancer dissemination programs.

12 NAs have crucial roles in control of EMT and EMT-associated traits such as migration, invasion and ch

13 ate with accessibility of key epithelial and EMT transcription factor binding sites.

14 mportant roles in prostatic inflammation and EMT and suggests the merit of further investigation to e

15 din-4 reinforce proliferation, invasion, and EMT in AGS, HGC-27, and SGC-7901 cells, which could be r

16 laying the regulation between the kinome and EMT require further elucidation to define targetable con

17 EMT-like and EMT-independent amoeboid cell subsets showed stable amoe

18 , how plasticity of tumor cell migration and EMT is spatiotemporally controlled and connected upon ch

19 thereby block TGF-beta-induced migration and EMT.

20 but was required for upregulation of p21 and EMT indicating a partial divergence between TGFbeta and

21 al priming in dictating tumor phenotypes and EMT.

22 dose-dependently inhibited proliferation and EMT of stimulated RPE cells by down-regulating Wnt (beta

23 tigation reveals that MAPK/ERK signaling and EMT-inducing transcription factor ZEB1 are critical to m

24 molecular network that controls stemness and EMT in glioblastoma, suggesting S100A4 as a candidate th

25 f chromatin at key metastasis suppressor and EMT genes, defining a new mechanism regulating cancer in

26 y networks associated with tumorigenesis and EMT that correlate with accessibility of key epithelial

27 an important therapeutic tool to antagonize EMT and cancer progression.

28 ute to detrimental TGFbeta signaling such as EMT.

29 ly that differential MAPK signaling balances EMT, cancer stem cell potential, and tumor growth in col

30 ed to account for possible crosstalk between EMT and non-EMT cells that promotes dissemination of non

31 and its use to explore relationships between EMT and the generation of cancer stem cells (CSCs) in pr

32 ay thus constitute a common endpoint of both EMT-dependent and EMT-independent cancer dissemination p

33 their expression is closely related to both EMT activity and airway obstruction.

34 that chlamydia-induced fibrosis is caused by EMT-driven generation of myofibroblasts, the effector ce

35 rther supports the DNM3OS and ovarian cancer EMT connection.

36 producible gene regulation in ovarian cancer EMT.

37 obstruction and to expression of a canonical EMT biomarker (S100A4).

38 I inhibitors would act against non-canonical EMT-induced GLI activation.

39 ifically in beta-cells ameliorated beta-cell EMT and beta-cell loss and prevented the onset of diabet

40 ymal morphogenesis and expression of certain EMT markers.

41 properties, but the mechanism(s) connecting EMT programs to stemness remain unclear.

42 naling, but with the absence of conventional EMT markers.

43 l role in cell migration, SMAD7 degradation, EMT, and induction of beta-catenin, and all of these pat

44 e precise mechanisms by which ZEB1-dependent EMT promotes malignancy remain largely undefined.

45 n that, rather than causing Golgi dispersal, EMT led to the formation of compact Golgi organelles wit

46 loop between Snail-nuclear Cat L-CUX1 drives EMT, which can be antagonized by Z-FY-CHO.

47 the roles of mature miRNA biogenesis during EMT process needs to be defined.

48 to the regulation of EpCAM expression during EMT, demonstrate an unexpected role for EpCAM in the reg

49 Autophagic flux impairment during EMT-mediated CD44L to CD44H cell conversion in vitro ind

50 , we monitored centrosome positioning during EMT in vivo, in developing mouse embryos and mammary gla

51 VM and suggest that miRNAs repressed during EMT, in addition to suppressing migratory and stem-like

52 ZIP6 levels are five-fold upregulated during EMT and the protein forms a complex with NCAM1.

53 y controlling N-cadherin upregulation during EMT.

54 gether, our results suggest that ECs enhance EMT-induced TNBC cell metastasis via PAI-1 and CCL5 sign

55 We examined EMT-competent lung epithelial cells and lung fibroblasts

56 ranscription factors, ZEB1 and ZEB2, execute EMT programs in embryonic development and cancer.

57 F) stem cell-derived SCCs frequently exhibit EMT, efficiently form secondary tumors, and possess incr

58 mesenchymal carcinoma cell lines exhibiting EMT markers expressed low levels of MHC-I, high levels o

59 osed to trastuzumab and pertuzumab expressed EMT markers and were poorly differentiated, whereas tumo

60 he identity and function of cells expressing EMT-associated genes in normal murine mammary gland home

61 hese data suggest that autophagy facilitates EMT-mediated CD44H generation via modulation of redox ho

62 ted that overexpression of RGC32 facilitates EMT of CRC cells by activating Smad/Sip1 signaling.

63 high grade mammary carcinomas with bona fide EMT, histologically similar to human metaplastic breast

64 miR-200, a family of microRNAs critical for EMT, in EAC cell lines.

65 ent oligomerization of ILEI is essential for EMT and tumor progression in vivo The structures and the

66 y, that not all cells having a potential for EMT exhibit stem cell-like properties.

67 gamma or talin or their interaction impaired EMT and the acquisition of cell motility and stemness.

68 ls a critical Dub3-Snail1 signalling axis in EMT and metastasis, and provides an effective therapeuti

69 This review elucidates the role of AXL in EMT-mediated oncogenesis and highlights the reciprocal c

70 ted with downregulation of genes involved in EMT, tumor invasion, and metastasis.

71 l for tumor cell migration and metastasis in EMT-driven lung adenocarcinoma models.

72 re, we report the novel functions of PHF8 in EMT (epithelial to mesenchymal transition) and breast ca

73 s junction proteins was lost with increasing EMT phenotype.

74 is work revealed that TGFbeta did not induce EMT in PC9 cells, but rather TGFbeta-inhibition induced

75 cancer cells in vivo, STAT4 failed to induce EMT directly in vitro, suggesting that STAT4 might media

76 regulation during Ras- and TGF-beta-induced EMT that involves alterations of accessible chromatin, w

77 GA1 is required for TGFbeta/collagen-induced EMT and metastasis.

78 knockdown prevents DICER1 depletion-induced EMT despite global microRNA (miRNA) downregulation.

79 dence of a novel role for PAK4 in IR-induced EMT and suggest potential therapeutic efficacy of target

80 KLF10 functions to suppress TGFbeta-induced EMT, establishing a molecular basis for the dichotomy of

81 owth signal CDK2 and ablated TGFbeta-induced EMT.

82 ed that increased expression of XRN2 induced EMT and promoted metastasis in vitro and in vivo.

83 activating TGFbeta signaling, which induces EMT.

84 nction of GM-CSF in colon cancer by inducing EMT.

85 semination from the primary site by inducing EMT/CSC phenotype.

86 ng to suppress Slug transcription to inhibit EMT.

87 In keratinocytes, SIRT1 knockdown inhibited EMT, cell migration, and TGF-beta signaling.

88 ma and glioma stem cells similarly inhibited EMT and induced MET, arguing that HCMV induces an epithe

89 Initial EMT was induced by prolonged exposure to IL6, a cytokine

90 Wnt signaling initiates EMT, whereas FGF signaling terminates this event.

91 ic carcinomas and sarcomas with intermediate EMT features.

92 Whether invasive tumor phenotypes like EMT arise from oncogenic drivers or from priming of the

93 on (EMT) by driving expression of the master EMT regulators and stem cell markers.

94 100A4 is an upstream regulator of the master EMT regulators SNAIL2 and ZEB along with other mesenchym

95 n vitro, suggesting that STAT4 might mediate EMT process via cancer-stroma interactions.

96 Concurrently, TGFbeta drives Notch1-mediated EMT to generate tumor initiating cells characterized by

97 IR as a crucial player in the Snail-mediated EMT.

98 ndent ( approximately 70%) of Twist-mediated EMT.

99 ters, and that this SPZ1-TWIST axis mediates EMT signaling and exerts significant regulatory effects

100 sor SNAI2, each crucial factors in mediating EMT.

101 ression in breast cancer cells increased MEK-EMT (MEK-epithelial-to-mesenchymal transition) signaling

102 ough induction of EMT, indicating IL-17-MMP7-EMT axis as a potential target for developing new strate

103 In breast cancer models, EMT cells induce increased metastasis of weakly metastat

104 We show that a molecular EMT signature can be experimentally induced in healthy h

105 that ZNF326 regulated expression of multiple EMT and cancer stem cell (CSC) pathway genes.

106 t for possible crosstalk between EMT and non-EMT cells that promotes dissemination of non-EMT cells.

107 creased metastasis of weakly metastatic, non-EMT tumour cells in a paracrine manner, in part by non-c

108 EMT cells that promotes dissemination of non-EMT cells.

109 his approach, we defined miR-520f as a novel EMT-reversing miRNA.

110 romoter and indirectly through activation of EMT-associated transcription factors SNAI1, SNAI2, TWIST

111 e used to further interrogate the biology of EMT in prostate cancer.

112 w doses of radiation (LDR) in the context of EMT has not yet to be thoroughly explored.

113 that miRNAs have crucial roles in control of EMT and EMT-associated traits such as migration, invasio

114 spectrum, to investigate the correlation of EMT score with cancer treatment response and survival, a

115 ed, this study delineates the development of EMT-positive mCSCs in HCC-free liver tissue upon chronic

116 rming growth factor-beta1, a major driver of EMT.

117 Investigating the collaborative effect of EMT and ECM in the metastatic process reveals increased

118 Although the cell-intrinsic effects of EMT are important for tumor progression, the reciprocal

119 ensitivity data indicated that enrichment of EMT features was associated with increased sensitivity t

120 endency to associate with gene enrichment of EMT, while miR-200c did not, in TCGA cohort, and our fin

121 ion of TGFbeta correlated with expression of EMT-related genes, and we found an inverse correlation b

122 ced cell proliferation and the expression of EMT-related genes.

123 of morphology, stiffness, and expression of EMT/myofibroblast markers and fibrillar collagens.

124 KLF10 depletion accentuated induction of EMT as assessed by multiple metrics.

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

126 specimens in vivo and following induction of EMT in cancer cell lines in vitro.

127 etastasis of ovarian cancer via induction of EMT program.

128 Chlamydial induction of EMT resulted in the generation of alpha-smooth muscle ac

129 Moreover, induction of EMT within primary human eSCs can be prevented and even

130 prostate carcinogenesis through induction of EMT, indicating IL-17-MMP7-EMT axis as a potential targe

131 , which was concurrent with the induction of EMT, migration, invasion and metastasis of these cells.

132 Furthermore, the inhibition of EMT prevented the generation of myofibroblasts and produ

133 ndent manner, which results in inhibition of EMT.

134 ion and invasion via phenotypic inversion of EMT, correlated with increased expression of E-cadherin

135 n vitro model, suggesting the involvement of EMT in diabetic cataract formation.

136 e development of a new, spontaneous model of EMT which involves four phenotypically distinct clones d

137 towards a contribution of the modulation of EMT.

138 as the others contained large populations of EMT-derived, vimentin-positive cells having spindle-like

139 The range of EMT scores in UCS was the largest among all tumor types

140 portant role of miR-218 in the regulation of EMT-related traits and metastasis of lung cancer in part

141 nd ERK that contributes to the regulation of EMT.

142 ranscription factor Slug, a key regulator of EMT.

143 previous reports of S100A4 as a reporter of EMT, we discovered that S100A4 is an upstream regulator

144 The repression of EMT genes was dependent on early viral gene expression a

145 In contrast, the precise role of EMT-related processes in tumors originating from mesench

146 stem and define stromal interactions and a p-EMT program associated with metastasis.

147 nt and stromal composition and established p-EMT as an independent predictor of nodal metastasis, gra

148 Cells expressing the p-EMT program spatially localized to the leading edge of p

149 tial epithelial-to-mesenchymal transition (p-EMT).

150 , yet remains critical for the pathological, EMT-inducing arm of TGFbeta signaling.

151 verse factors have been identified as potent EMT inducers in ovarian cancer.

152 , we demonstrated the relevance of predicted EMT scores to patient survival and observed that the rol

153 ween TGFbeta and EGFR signalling may prevent EMT progression in this context rather than promote it.

154 abolic tumor suppressor in PCa that prevents EMT and the Warburg effect, and indicates that ABHD5 is

155 repression leads to CRC cell proliferation, EMT, and tumorigenesis.

156 e show that VEGFA induction of Sox2 promotes EMT and tumor metastasis.

157 ermatogenic leucine zipper 1 (SPZ1) promotes EMT through its transactivating ability in increasing TW

158 Exogenous TGFbeta promotes EMT in a unique pathway of PRMT5-MEP50 catalyzed histone

159 ome-wide mapping shows 73% of MEG3-regulated EMT-linked pathway genes contain MEG3 binding sites.

160 ively, our study uncovers REST in regulating EMT and stemness properties of NE PCa cells and suggests

161 act, and upregulation of miR-30a can repress EMT through its targeting of SNAI1 in lens epithelial ce

162 Snail and the E-cadherin promoter, reversed EMT, and decreased cell migration/invasion.

163 cks cellular growth via apoptosis, reversing EMT-signaling and impairing mammosphere formation, there

164 Prior work showed EMT transcription factor overexpression upregulates CSC.

165 Fbeta-VAV1 signalling decreased the squamous/EMT-like cancer cells, promoted nuclear VAV1 localizatio

166 amma-mediated Nox1 expression and suppressed EMT in IR-treated cells.

167 /EPS8/ABI1 complex is critical for sustained EMT traits of ovarian cancer cells.

168 However, molecular mechanism sustaining EMT of ovarian cancer cells remains elusive.

169 ngs may provide useful avenues for targeting EMT or specific components of the EMT pathways as a ther

170 It is concluded that EMT is involved in human diabetic cataract, and upregula

171 Our findings indicate that EMT contributes to metastasis via non-cell autonomous ef

172 We observe that EMT silences protective mucosal interferon (IFN)-I and I

173 Further experiments also reveal that EMT can be induced in epithelial-like ovarian cancer cel

174 Here, we show that EMT also occurs within the bulge, the epithelial stem ce

175 Our data suggest that EMT does not contribute directly to the myofibroblast po

176 g ADAM9, the TGFbeta receptor TGFBR2 and the EMT inducers ZEB1, ZEB2, and the snail transcriptional r

177 procal control between AXL signaling and the EMT state.

178 d cell migration and invasion as well as the EMT process.

179 receptor-gamma agonists also attenuates the EMT signature even in lesional lichen planopilaris hair

180 epression of E-cadherin transcription by the EMT inducers Snail1 and Zeb2 plays a fundamental role in

181 Induced by the EMT, zinc finger E-box binding homeobox 1 (ZEB1) binds a

182 Knockdown of NFkappaB decreased the EMT phenotypes and metastatic capacity of these cells.

183 phenotype by regulating key elements in the EMT signaling axis.

184 prevent activation of STAT3 and inhibit the EMT and metastasis.

185 targeting EMT or specific components of the EMT pathways as a therapeutic intervention strategy to p

186 eated beta-cells activated expression of the EMT regulator gene Snail in a SMAD3/Stat3-dependent mann

187 of LOXL2 action with elevated levels of the EMT regulatory transcription factor Snail1 and expressio

188 Ectopic expression of the EMT-activating transcription factor ZEB1 stimulated Golg

189 lgorithm is a promising tool to quantify the EMT spectrum, to investigate the correlation of EMT scor

190 Recently, the EMT gradient has also been shown to rewire the kinase si

191 In human breast tumours, the EMT-transcription factors strongly correlate with activa

192 RNA blocked albumin-induced changes in these EMT markers as well.

193 assay for the simultaneous analysis of three EMT-associated genes miR-200c/141, miR-200b/a/429 and CD

194 stalk between CXCR4 and CXCR2 contributed to EMT, migration and invasion of gastric cancer.

195 pressing constitutively active Rac1 leads to EMT in epithelial-like ovarian cancer cells.

196 that cells can be stably halted en route to EMT in a hybrid E/M phenotype.

197 tional states differentially prime tumors to EMT.

198 as the epithelial-to-mesenchymal transition (EMT) [7, 8].

199 including epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) acquisitions.

200 volved in epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) maintenance resulting in

201 5 induced epithelial-mesenchymal transition (EMT) and disrupted epithelial cell polarity, which was a

202 reased epithelial-to-mesenchymal transition (EMT) and enhanced tumor cell dissemination in adjacent b

203 cilitated epithelial-mesenchymal transition (EMT) and epithelial cell migration.

204 egulating epithelial-mesenchymal transition (EMT) and establish ZEB2 as a novel regulator of AML prol

205 elated epithelial-to-mesenchymal transition (EMT) and poor chemotherapy response.

206 linked to epithelial-mesenchymal transition (EMT) and promoting cell survival, anoikis resistance, in

207 volved in epithelial-mesenchymal transition (EMT) and stemness acquisition in NE differentiated prost

208 ated upon epithelial-mesenchymal transition (EMT) and together with the cytoskeletal protein talin as

209 ation and epithelial-mesenchymal transition (EMT) are coupled to promote SCC tumor initiation in conc

210 T) and epithelial-to-mesenchymal transition (EMT) are important processes in kidney development.

211 ulated an epithelial-mesenchymal transition (EMT) as indicated by the decrease in epithelial marker E

212 HCC cell epithelial-mesenchymal transition (EMT) as well.

213 nduces epithelial-to-mesenchymal transition (EMT) by acting as a molecular sponge of miR-566.

214 ces an epithelial-to-mesenchymal transition (EMT) by driving expression of the master EMT regulators

215 rgo an epithelial-to-mesenchymal transition (EMT) following transformation acquire CSC properties.

216 ng the epithelial to mesenchymal transition (EMT) from NMP to mesodermal progenitor.

217 strong epithelial-to-mesenchymal transition (EMT) gene signature in a subset of cases that was attrib

218 ion in epithelial-to-mesenchymal transition (EMT) has been linked to the TKI resistance in lung adeno

219 Epithelial-to-mesenchymal transition (EMT) has been proposed as one mechanism afflicting barri

220 Epithelial-mesenchymal transition (EMT) has been recognized as a key element of cell migrat

221 d that epithelial to mesenchymal transition (EMT) in breast cancer cells regulates metastasis, stem c

222 a loss of epithelial-mesenchymal transition (EMT) in BVE(Cyp24a1-null) cells, associated with downreg

223 Epithelial to mesenchymal transition (EMT) in cancer cells has been associated with metastasis

224 ersing epithelial-to-mesenchymal transition (EMT) in cancer cells has been widely considered as an ap

225 ing an epithelial-to-mesenchymal transition (EMT) in cancer cells to promote tumor progression.

226 cilitated epithelial-mesenchymal transition (EMT) in CRC via the Smad/Sip1 signaling pathway, as show

227 ducers of epithelial-mesenchymal transition (EMT) in cystine-independent breast cancer cells conferre

228 ng and epithelial-to-mesenchymal transition (EMT) in human CRC cell lines of varying stages of differ

229 markers, epithelial-mesenchymal transition (EMT) inducers and basal-enriched molecules, while cluste

230 The epithelial-to-mesenchymal transition (EMT) is a cell biological program that confers mesenchym

231 Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process in de

232 Epithelial-mesenchymal transition (EMT) is an important biological process that has been im

233 The epithelial-mesenchymal transition (EMT) is an important process in the progression of cance

234 Epithelial-to-mesenchymal transition (EMT) is critical for embryonic development and wound hea

235 Epithelial-mesenchymal transition (EMT) is induced by transforming growth factor (TGF)-beta

236 ion of epithelial-to-mesenchymal transition (EMT) markers were performed on human cancer cells treate

237 ion of epithelial-to-mesenchymal transition (EMT) markers ZEB1, ZEB2 and CDH2 (which encodes N-cadher

238 es the epithelial-to-mesenchymal transition (EMT) of lung cancer cells by directly repressing the exp

239 ducing epithelial-to-mesenchymal transition (EMT) of ovarian cancer cells in vivo, STAT4 failed to in

240 ation and epithelial mesenchymal transition (EMT) of retinal pigment epithelium (RPE).

241 on of the epithelial-mesenchymal transition (EMT) program and self-renewal traits (CSCs) via various

242 es in the epithelial-mesenchymal transition (EMT) program.

243 both use epithelial-mesenchymal transition (EMT) programs to acquire SC properties, but the mechanis

244 rgo an epithelial-to-mesenchymal transition (EMT) regulated by various transcription factors, includi

245 d with epithelial-to-mesenchymal transition (EMT) remains unclear.

246 hanced epithelial-to-mesenchymal transition (EMT) signature after USF3 knockdown or USF3 p.[Gln1478de

247 n induces epithelial-mesenchymal transition (EMT) state and cancer stem-like cell (CSC) properties in

248 nduced epithelial-to-mesenchymal transition (EMT) through activation of zinc finger E-box binding hom

249 ion of epithelial-to-mesenchymal transition (EMT) to the profibrotic stiff microenvironment and myofi

250 genes, epithelial-to-mesenchymal transition (EMT) transcription factors and hypoxia-inducible-factor

251 and an epithelial to mesenchymal transition (EMT) transcriptional program.

252 of the epithelial to mesenchymal transition (EMT) using flow cytometry, immunofluorescence, and quant

253 ncer cell epithelial-mesenchymal transition (EMT) was inhibited, accompanied with inhibition in metas

254 fibrotic endothelial-mesenchymal transition (EMT) which was reversed back to an endothelial phenotype

255 icipating epithelial-mesenchymal transition (EMT), a critical cellular event for metastasis of malign

256 lating epithelial-to-mesenchymal transition (EMT), a key mechanism enabling epithelial tumor cells to

257 ntrols epithelial-to-mesenchymal transition (EMT), a reversible embryonic transdifferentiation progra

258 rocess of epithelial mesenchymal transition (EMT), an intermediate between smoking and airway fibrosi

259 underwent epithelial-mesenchymal transition (EMT), and expressed markers related to colon cancer stem

260 of the Epithelial-to-Mesenchymal Transition (EMT), from which we identified four experimentally obser

261 moting epithelial-to-mesenchymal transition (EMT), invasiveness and metastasis.

262 factor of epithelial-mesenchymal transition (EMT), is subjected to ubiquitination and degradation, bu

263 ers of epithelial-to-mesenchymal transition (EMT), or MIR34A or was associated with metastasis.

264 o induce endothelial-mesenchymal transition (EMT), TNBC cells could produce plasminogen activator inh

265 during epithelial-to-mesenchymal transition (EMT), we investigated ZIP6 in an EMT paradigm using ZIP6

266 RNA to epithelial-to-mesenchymal transition (EMT), which correlates with metastasis.

267 by the epithelial-to-mesenchymal transition (EMT)-a dynamic process characterized by phenotypic and m

268 ulates an epithelial-mesenchymal transition (EMT)-associated CD44 isoform switch in a G-quadruplex-de

269 uamous/epithelial-to-mesenchymal transition (EMT)-like subtype.

270 ion of epithelial-to-mesenchymal transition (EMT)-related molecules further point towards a contribut

271 e, and epithelial-to-mesenchymal transition (EMT).

272 artial epithelial-to-mesenchymal transition (EMT).

273 vement of epithelial-mesenchymal transition (EMT).

274 ramme: epithelial-to-mesenchymal transition (EMT).

275 lation epithelial-to-mesenchymal transition (EMT).

276 ted to epithelial-to-mesenchymal transition (EMT).

277 induce epithelial-to-mesenchymal transition (EMT).

278 nce of epithelial to mesenchymal transition (EMT).

279 during epithelial-to-mesenchymal transition (EMT).

280 ted to epithelial-to-mesenchymal transition (EMT).

281 n-like epithelial-to-mesenchymal-transition (EMT) inducer (ILEI) has been shown to be strongly up-reg

282 mitigated epithelial-mesenchymal-transition (EMT), as well as enhanced fibrinolysis and impaired angi

283 light that effector-to-memory transitioning (EMT) CD4(+) T cells are particularly permissive for the

284 ymal and mesenchymal-epithelial transitions (EMT/MET) and phenotypically recapitulate the metastatic

285 ow VGF can confer TKI resistance and trigger EMT, suggesting its potential utility as a biomarker and

286 One of the two EMT-negative clones exhibited aggressive stem cell-like

287 One of the two EMT-positive clones exhibited aggressive and stem cell-l

288 reported that lens epithelial cells undergo EMT during cataract formation, and regulation of microRN

289 isposing squamous cell carcinomas to undergo EMT and metastasis, suggesting that the pre-tumor epigen

290 Some tumors undergo EMT while others do not, which may reflect intrinsic pro

291 In contrast, cells undergoing EMT failed to reach the values exhibited by IPF myofibro

292 ary cells treated with TGFbeta or undergoing EMT upregulated CD73 cell-surface expression, confirming

293 y, we show that once NC cells have undergone EMT, the same PDGF-A/PDGFRalpha works as an NC chemoattr

294 gands for the TGFbeta receptor and underwent EMT.

295 ggest that UCSs do not develop from EACs via EMT.

296 d Pten double KO mice recapitulated the weak EMT characteristics observed in Mmp7(-/-) mice.

297 al novel therapeutic avenue in cancers where EMT and CD44H cells have been implicated, including ESCC

298 ds to the initiation of Wilms tumor, whereas EMT contributes to the development of renal cell carcino

299 al that cystine-addiction is associated with EMT in breast cancer during tumor progression.

300 lly, high PAQR11 levels were correlated with EMT and shorter survival in human cancers, and PAQR11 wa