ライフサイエンスコーパス: EMT

1 EMT is crucial to embryonic development and wound healin

2 EMT is often related with acquisition of stemness charac

3 EMT may potentially be induced by inflammatory cytokines

4 EMT occurs in a diverse range of physiological and patho

5 EMT tumors preferentially used the nucleotide salvage pa

6 EMTs are driven by SNAIL, ZEB and TWIST transcription fa

7 in the Suit2 line was sufficient to activate EMT pathways.

8 als controlling cancer cell plasticity along EMT and suggests that hybrid and mesenchymal phenotypes

9 he outcome of a 2-year-long discussion among EMT researchers and aims to both clarify the nomenclatur

10 dinated by increased expression of ZEB-1, an EMT activator.

11 Here we describe an EMT-like process that requires tissue-level coordination

12 ence of EMT in metastasis, we established an EMT lineage tracing (Tri-PyMT) model, in which tumor cel

13 ks) to explore the intermediate states of an EMT model network by computing summaries of the dynamics

14 RUNX1 within the eye for the treatment of an EMT-mediated condition using a topical ophthalmic agent.

15 giogenic endothelial cells (EC) regulates an EMT-like suite of target genes, and suppresses Dll4-Notc

16 y breast cancer cells that have undergone an EMT, promotes paracrine-mediated increases in proliferat

17 er metastasis showed drug-resistant CSC- and EMT-like phenotype with aerobic glycolysis and fatty aci

18 to support optimal inclusion development and EMT induction.

19 functional studies revealed that the EMT and EMT-associated phenotypes, including enhanced cell invas

20 but its role in infectivity, inclusions, and EMT induction is unknown.

21 on, data showed direct link between iron and EMT.

22 profiling focused on cancer progression and EMT, and metabolomics by mass spectrometry and cellular

23 y, which drives epigenomic reprogramming and EMT to counteract apoptosis.

24 es with activation of Hedgehog signaling and EMT in the human disease.

25 B-induced AKT/GSK3beta/Snail1 signaling and EMT that could be attenuated by Aurora B kinase inhibito

26 reversed SIX1-induced TGFbeta signaling and EMT.

27 Aberrant TGF-beta signalling and EMT are implicated in the pathogenesis of renal fibrosis

28 rlying the relationship between stemness and EMT programs, which may represent therapeutic vulnerabil

29 r cells, although reduced their stemness and EMT-like features, still formed tumors and lung metastas

30 We referred to this phenomenon as EMT memory.

31 sion of these inflammatory genes, as well as EMT, tumor cell proliferation, and migration in vitro an

32 The mRNA expression of TGF-beta (EMT-inducer) showed no significant alterations.

33 differences in nucleotide metabolism between EMT and papillary subtypes.

34 or other cell fate transition systems beyond EMT.

35 easing CFTR activity was sufficient to block EMT.

36 henotypes, including metastasis, imparted by EMT cells on adjacent epithelial cancer cells can be dis

37 signals during both developmental and cancer EMT programs.

38 and applying to twelve published single-cell EMT datasets in cancer and embryogenesis, we uncover the

39 pancreatic cancer cells up-regulate classic EMT regulator Slug, providing a link between nutrient st

40 GFbeta1)-induced deacetylation of contactin, EMT, phosphorylation of Smad3, STAT3, and beta-catenin,

41 astatic cells were used to evaluate the CSC, EMT (epithelial-to-mesenchymal transition), and metaboli

42 tokines by neutralizing antibodies decreased EMT and slowed lung cancer progression and metastasis.

43 rol in breast cancer cell dedifferentiation, EMT, and metastasis.

44 We describe EMT as a novel mechanism for infection-associated chorio

45 ow an interaction between cells in different EMT states confers properties that are not induced by ei

46 Thus, heterogeneous activation of distinct EMT programs promotes a mode of collective invasion that

47 in metabolic pathway utilization distinguish EMT and papillary subtypes of breast cancer and identify

48 als from the tumor microenvironment to drive EMT, invasion, and metastasis.

49 RNA-mediated mechanism for active AKT-driven EMT-independent LAD metastasis and indicates the great p

50 egradation of intermediate filaments driving EMT, resulting in cell death.

51 ocal adhesions, two features affected during EMT.

52 n modifications has been demonstrated during EMT.

53 tate aberrant growth factor signaling during EMT-associated drug resistance and metastasis.

54 atrix remodeling that are upregulated during EMT and are highly expressed in patients with aggressive

55 rther indicate that NRP1 upregulation during EMT is mediated via binding of the chromatin reader prot

56 h a powerful tool to investigate the dynamic EMT process in tumor biology.

57 rs properties that are not induced by either EMT program alone.

58 oring, cesarean section deliveries exhibited EMT after exposure to oxidative stress, and the pregnanc

59 the mechanism by which these SIX1-expressing EMT cells activate GLI signaling remained unclear.

60 nhibited estrogen-regulated gene expression, EMT, and distant metastasis in vivo, suggesting that AR

61 tent inducer of developmental and fibrogenic EMTs(4,9,10).

62 ed induction of developmental and fibrogenic EMTs.

63 e isoform switching of CLSTN1 is crucial for EMT.

64 e and provide definitions and guidelines for EMT research in future publications.

65 data, we propose a statistical mechanism for EMT in which many unobservable microstates may exist wit

66 s continue to express E-cadherin, and a full EMT is not always necessary for metastasis; also, positi

67 luripotency exit, whereas the latter, a full EMT, is associated with complete and irreversible plurip

68 Although gastrulation EMT coincides with loss of epiblast pluripotency, plurip

69 the invasion of proliferative DeltaNp63-high EMT cells in heterogeneous primary tumors.

70 A DeltaNp63-high EMT program coupled the ability to proliferate with an I

71 ctions through inhibition of the Fli-1/HSPB1/EMT/ECM remodeling protein networks.

72 icroenvironmental signals controlling hybrid EMT phenotypes and indicate that EMT involves multiple m

73 as a splicing regulatory factor that impedes EMT and breast cancer metastasis.

74 be disrupted by either inhibiting VEGF-C in EMT cells or by knocking down NRP2, a receptor which int

75 ls precisely marked an unequivocal change in EMT status, defining the pre-EMT and post-EMT compartmen

76 se attenuation, and transition efficiency in EMT, and reveal their trade-off relations.

77 n not only restored E-cadherin expression in EMT memory, but also primed cells for chemotherapy-induc

78 beta-activated SMAD transcription factors in EMT.

79 ction by highlighting a role for ST6Gal-I in EMT, which may be mediated, at least in part, by alpha2-

80 he expression profile of genes implicated in EMT and metastasis.

81 lls and certain cancers however, its role in EMT gene regulation is unknown.

82 mechanistic insight into ST6Gal-I's role in EMT, we examined the activity of epidermal growth factor

83 to be an early player, owing to its role in EMT.

84 ormalin fixed), being 0.9 nm smaller than in EMT cancer-invaded regions.

85 Multiple invasion pathways including EMT, bone morphogenetic protein (BMP) signaling, chemoki

86 poxia reduced C19MC expression and increased EMT genes.

87 ng known to require Ras activation to induce EMT.

88 These results suggest that TGF-beta induced EMT and cancer stemness acquisition could be associated

89 1)-based peptide inhibited chlamydia-induced EMT, revealing a major source of active TGF-beta during

90 r exposing them to the respective CM induced EMT in cancer cells and modulated the expression profile

91 PDAC cells for glutamine deprivation-induced EMT, cell motility, and nutrient stress survival.

92 egulation of Abi1 mediates PTEN loss-induced EMT and CSC activity.

93 rom a computational model of TGFbeta-induced EMT, can reconstruct the cell state and predict the timi

94 rowth, and responsiveness to TGFbeta-induced EMT.

95 These findings support that Aurora B induces EMT to promote breast cancer metastasis via OCT4/AKT/GSK

96 Interestingly, EMT is not a binary process but instead proceeds with mu

97 AP mechanotransduction signalling, involving EMT-like characteristics, resulting in robust heart rege

98 An irreversible EMT and the accumulation of AMCs characterize the amnion

99 lasticity during reversible and irreversible EMT.

100 fixed differentiation status of irreversible EMT.

101 dherin and altered the expression of the key EMT-mediating transcription factors.

102 ermal growth factor receptor (EGFR), a known EMT driver.

103 tantly, rare growth-suppressed DeltaNp63-low EMT cells influenced tumor progression by leading the in

104 An alternative DeltaNp63-low EMT program conferred cells with the ability to initiate

105 However, this DeltaNp63-low EMT state triggered a collateral loss of fitness.

106 effectively impair the function of a master EMT-transcriptional factor.

107 nstrating the plasticity of CBFbeta-mediated EMT.

108 ually progressing epithelial-to-mesenchymal (EMT) phenotype following a 21-day exposure to IL-1beta,

109 uch as during the epithelial-to-mesenchymal (EMT) transition in cancer, and therefore may serve as a

110 Misregulated EMT has been implicated in processes associated with can

111 To investigate whether activation of EMT and stem cell markers might be involved in epigeneti

112 Activation of EMT significantly increases production of hyaluronic aci

113 tastatic subclones had greater activation of EMT-related gene networks than parental Suit2 cells, and

114 ug resistance, no standardized assessment of EMT phenotypic heterogeneity in human carcinomas exists;

115 ed to evaluate functional characteristics of EMT and stemness acquisition.

116 view the key features and characteristics of EMT dynamics, with a focus on the mathematical modeling

117 process in cancer progression downstream of EMT.

118 G was indispensable for the establishment of EMT memory.

119 and patient samples, we provide evidence of EMT in endometriosis.

120 To obtain in vivo evidence of EMT in metastasis, we established an EMT lineage tracing

121 that P-TEFb also controls the expression of EMT regulators to promote breast cancer progression.

122 derstanding of the dynamics and functions of EMT plasticity during cancer metastasis.

123 RUNX1 upregulation was a hallmark of EMT in primary cultures derived from human PVR membranes

124 Snail, master inducer of EMT, requires HOTAIR to recruit EZH2 on specific epithel

125 th NRPs, which is enhanced upon induction of EMT.

126 NGS revealed changes in expression levels of EMT markers (E-cadherin, N-cadherin, fibronectin, viment

127 migratory packs, and mesenchymal markers of EMT remain unapparent.

128 First, by fitting a hidden Markov model of EMT with experimental data, we propose a statistical mec

129 overexpression of SNAI1, a key modulator of EMT, is a pathologically relevant event in human acute m

130 The gene networks of EMT, angiogenesis, immune-suppression and T cell exhaust

131 s in contrast to the classical perception of EMT as leading to a binary choice.

132 ithelial-like morphology, down-regulation of EMT characteristics, and loss of cancer stemness feature

133 igate the role of C19MC in the regulation of EMT genes, we employed the CRISPR/dCas9 Synergistic Acti

134 ion, and adopting a phenotype reminiscent of EMT.

135 Despite the role of EMT in metastasis and drug resistance, no standardized a

136 hymal transition (EMT), although the role of EMT in metastasis remains controversial.

137 Elucidating the role of EMT will improve the understanding of the molecular mech

138 The functional roles of EMT, MET, and the partial state (referred to as pEMT) ma

139 t the Tri-PyMT cells exhibited a spectrum of EMT phenotypes, with EMT-related genes concomitantly exp

140 During the initial stages of EMT, there was a gradual decrease in E-cadherin force an

141 C19MC cistron and resulted in suppression of EMT associated genes.

142 CAFs resulted in significant upregulation of EMT markers, while myCAFs reverted this phenotype.

143 e (MAPK) pathway inputs for the induction of EMTs(12-19).

144 Most studies have so far focused on EMT involving single or isolated groups of cells.

145 holo-transferrin 0-2 g/L for 24 and 48 h) on EMT biomarkers in the liver-derived HepG2 cells was inve

146 by Web of Science in 2019 alone, research on EMT is expanding rapidly.

147 cancer cells that had undergone an oncogenic EMT could increase metastasis of neighboring cancer cell

148 EPN3-induced partial EMT is instrumental for the transition from in situ to i

149 Moreover, the appearance of partial EMT or mesenchymal-like carcinoma cells in MDA-MB-468 tu

150 ral question about how the number of partial EMT states affects cell transformation.

151 ntermediate state traps cells in one partial EMT state.

152 epithelial state to intermediate or partial EMT state(s) to a mesenchymal state.

153 Here, we triggered partial EMT (pEMT) or UJT in differentiated primary human bronch

154 econdary tumors, suggesting their persistent EMT plasticity.

155 in EMT status, defining the pre-EMT and post-EMT compartments within the tumor.

156 differential contributions of pre- and post-EMT tumor cells in breast cancer metastasis.See related

157 Importantly, the post-EMT (GFP(+)) cells in the Tri-PyMT model were not perman

158 dominant roles in metastasis, while the post-EMT cells were supportive in promoting tumor invasion an

159 2 expression, suggesting that this potential EMT-inducing gene, is a responsive target of NFkB.

160 vocal change in EMT status, defining the pre-EMT and post-EMT compartments within the tumor.

161 Consistently, the pre-EMT cells played dominant roles in metastasis, while the

162 reduced inclusions by over 90% and prevented EMT induction.

163 ic inhibition of SLUG upregulation prevented EMT following the acute IL-1beta exposure but did not re

164 y addressed major concerns with the Tri-PyMT EMT lineage tracing model, which provides us with a powe

165 RPC4046 significantly reduced EMT markers in adults with active EoE, with greater effe

166 onstrate that glutamine deficiency regulates EMT through the up-regulation of the EMT master regulato

167 nsitive EPHA2/LYN protein complex regulating EMT and metastasis in response to increasing ECM stiffne

168 RFP-to-GFP switch of this model in reporting EMT of metastatic tumor cells.

169 ker vimentin (V) at subcellular resolution ("EMT-IFA").

170 s that determine the nature of the resulting EMT.

171 acute IL-1beta exposure but did not reverse EMT memory.

172 sses AKT/GSK3beta/Snail1 signaling, reverses EMT and reduces breast cancer metastatic potential in vi

173 bitor of the SIX1/EYA2 complex that reverses EMT phenotypes suppressing breast cancer metastasis.

174 dynamic cell state transitions of reversible EMT and the fixed differentiation status of irreversible

175 Herein, we review EMT, MET, pEMT, and plasticity in the context of tumor m

176 for optimal inclusion development and stable EMT induction.

177 ward AKT, not SMAD, which activated stemness/EMT phenotypes.

178 ing growth factor-beta (TGF-beta) stimulated EMT in a manner that depended on TGF-beta-activated kina

179 s immediate application, we used it to study EMT gene activity from the local primary tumor to a dist

180 Epiblast MET and its subsequent EMT are two distinct processes.

181 n and uncovers its novel role in suppressing EMT genes critical for maintaining the epithelial cytotr

182 Fbeta-dependent autocrine loop that sustains EMT.

183 typic characterization have established that EMT is a multistable process wherein cells exhibit and s

184 ling hybrid EMT phenotypes and indicate that EMT involves multiple molecular programs.

185 The EMT markers assessed were Snail-1, Snail-2, N-cadherin,

186 er of intermediate states can accelerate the EMT process and that adding parallel paths or transition

187 ntrol cancer-associated phenotypes along the EMT continuum, we defined a logical model of the EMT cel

188 tenuating Wnt/beta-catenin signaling and the EMT process.

189 This Consensus Statement, mediated by 'the EMT International Association' (TEMTIA), is the outcome

190 es of cytoskeleton disruption and during the EMT.

191 eterogeneity in human carcinomas exists; the EMT-IFA allows for clinical monitoring of tumor adaptati

192 st that HDAC8 activation is required for the EMT and renal fibrogenesis by activation of multiple pro

193 that is dependent on SIX1 expression in the EMT cancer cells.

194 the multistability is broadly present in the EMT network across parameters and thus response of cells

195 suppressor PTEN has been shown to induce the EMT, but the underlying molecular mechanisms are less un

196 continuum, we defined a logical model of the EMT cellular network that yields qualitative degrees of

197 confirm the fidelity and sensitivity of the EMT lineage tracing (Tri-PyMT) model and highlight the d

198 lloproteinases (MMPs) as well as some of the EMT markers tested.

199 gulates EMT through the up-regulation of the EMT master regulator Slug, a process that is dependent o

200 ent work has found that the d-spacing of the EMT positive breast cancer tissue (FFPE (dewaxed)) is wi

201 the MET can be reversed by expression of the EMT transcription factor Slug whose expression is depend

202 pable of inhibiting splicing activity of the EMT-promoting splicing regulator hnRNPM through protein-

203 Unexpectedly, nuclear expression of the EMT-TF ZEB2 in human primary melanoma has been shown to

204 ity of PTEN accounts for the reversal of the EMT.

205 LYN phosphorylates the EMT transcription factor TWIST1 to release TWIST1 from i

206 n vitro functional studies revealed that the EMT and EMT-associated phenotypes, including enhanced ce

207 enew and give rise to new tumors through the EMT.

208 This EMT is functionally different from that coordinated by t

209 This EMT-like process occurs along a continuous front in the

210 rophages, while promoting metastasis through EMT and endothelial activation.

211 ial-mesenchymal transition (EMT), leading to EMT induction in a kinase-dependent manner.

212 nchymal-epithelial transition (MET) prior to EMT-associated pluripotency loss.

213 pression, epithelial-mesenchymal transition (EMT) and angiogenesis as the key events and potentially

214 dependent epithelial-mesenchymal transition (EMT) and beta-catenin nuclear translocation to promote c

215 ducing epithelial to mesenchymal transition (EMT) and IKKalpha-dependent inflammatory genes, includin

216 , such as epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET), in pri

217 ) induced epithelial-mesenchymal transition (EMT) and migration in both primary human lung cancer cel

218 ducing an epithelial-mesenchymal transition (EMT) and stemness features.

219 ypes, the epithelial-mesenchymal transition (EMT) and the papillary subtypes.

220 The epithelial-to-mesenchymal transition (EMT) and the unjamming transition (UJT) each comprises a

221 te to the epithelial-mesenchymal transition (EMT) and tumor metastasis.

222 ndergo epithelial-to-mesenchymal transition (EMT) as they differentiate into invasive extravillous tr

223 on in the epithelial-mesenchymal transition (EMT) community.

224 opment of epithelial-mesenchymal transition (EMT) coordinated by increased expression of ZEB-1, an EM

225 Epithelial-mesenchymal transition (EMT) encompasses dynamic changes in cellular organizatio

226 forded by epithelial-mesenchymal transition (EMT) for cancer progression and drug resistance remains

227 Epithelial-to-mesenchymal transition (EMT) has been associated with cancer cell heterogeneity,

228 ted as an epithelial-mesenchymal transition (EMT) has been identified as a major obstacle for the eff

229 ors of epithelial-to-mesenchymal transition (EMT) have recently emerged as novel players in the field

230 o induced epithelial-mesenchymal transition (EMT) in lung cancer cells and promoted metastatic spread

231 uction of epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma (PDAC) cells.

232 ion of epithelial-to-mesenchymal transition (EMT) in the establishment of metastases is still controv

233 lators of epithelial-mesenchymal transition (EMT) including E-cadherin, Snail, Slug, and Twist2, in t

234 Epithelial to mesenchymal transition (EMT) is a dynamic process that drives cancer cell plasti

235 Epithelial-mesenchymal transition (EMT) is a fundamental biological process that plays a ce

236 Epithelial-to-mesenchymal transition (EMT) is a fundamental cellular process and plays an esse

237 The epithelial-mesenchymal transition (EMT) is a process by which cells lose epithelial traits,

238 The epithelial-mesenchymal transition (EMT) is an embryonic program frequently reactivated duri

239 nce of epithelial-to-mesenchymal transition (EMT) markers.

240 with the epithelial mesenchymal transition (EMT) occurs frequently during tumor metastasis.

241 omotes an epithelial-mesenchymal transition (EMT) phenotype and sensitizes PDAC cells to a clinical i

242 nduced an epithelial-mesenchymal transition (EMT) phenotype in tumor cells without affecting tumor-in

243 ed by the epithelial-mesenchymal transition (EMT) program.

244 The epithelial-mesenchymal transition (EMT) programs promote SC and CSC stemness in many epithe

245 ound that epithelial-mesenchymal transition (EMT) ranked first in the Hallmark pathway enrichment.

246 An epithelial-mesenchymal transition (EMT) represents a basic morphogenetic process of high ce

247 vasive epithelial-to-mesenchymal transition (EMT) states in subpopulations that establish a leader-fo

248 rd to the epithelial mesenchymal transition (EMT) structural component in malignant tissue.

249 ndergo epithelial to mesenchymal transition (EMT) to form contractile membranes within the eye.

250 nomas, epithelial-to-mesenchymal transition (EMT) upregulates LARP6 expression to enhance protein syn

251 ole in epithelial to mesenchymal transition (EMT) using the Suit2 pancreatic cancer cell line, which

252 ofile and epithelial-mesenchymal transition (EMT) were investigated using zymography and real-time qP

253 nduced an epithelial-mesenchymal transition (EMT) with cells exhibiting enhanced migration and invasi

254 t with epithelial to mesenchymal transition (EMT) with loss of epithelial (E-cadherin) and gain of me

255 uring the epithelial-mesenchymal transition (EMT), a process that promotes metastasis.

256 of the epithelial-to-mesenchymal transition (EMT), a transdifferentiation process triggering metastas

257 rgo an epithelial-to-mesenchymal transition (EMT), although the role of EMT in metastasis remains con

258 stemness, epithelial-mesenchymal transition (EMT), and lung and lymphatic metastasis in GC cells.

259 omotes epithelial-to-mesenchymal transition (EMT), cell invasion, and metastasis.

260 artial epithelial-to-mesenchymal transition (EMT), followed by the establishment of a TGFbeta-depende

261 ulator of epithelial-mesenchymal transition (EMT), leading to EMT induction in a kinase-dependent man

262 lination, epithelial-mesenchymal transition (EMT), loss of sensation and neuropathic pain.

263 ect to epithelial-to-mesenchymal transition (EMT), mediated, in part, by the p38 mitogen-activated pr

264 eling and epithelial mesenchymal transition (EMT), provide mechanistic pathways contributing to the d

265 volves epithelial to mesenchymal transition (EMT), the basis of cancer phenotype acquisition.

266 to induce epithelial-mesenchymal transition (EMT), VAL exerts potent pro-invasive and pro-metastatic

267 gating epithelial-to-mesenchymal transition (EMT), we develop an integrative tool that combines unsup

268 uction of epithelial-mesenchymal transition (EMT), which included enhanced expression of fibroblast g

269 ession of epithelial-mesenchymal transition (EMT)-associated genes, including MMP-9 and Snail.

270 Epithelial-to-mesenchymal transition (EMT)-inducing transcription factors (TF) are well known

271 ing an epithelial-to-mesenchymal transition (EMT)-like phenotype that disrupts junctions and enhances

272 resent an epithelial-mesenchymal transition (EMT)-like regenerative response manifested by cytoskelet

273 esion and epithelial-mesenchymal transition (EMT).

274 on and epithelial to mesenchymal transition (EMT).

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

276 uction of epithelial-mesenchymal transition (EMT).

277 iological epithelial-mesenchymal transition (EMT).

278 s through epithelial-mesenchymal transition (EMT).

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

280 ed lethal epithelial-mesenchymal transition (EMT).

281 diated by epithelial-mesenchymal transition (EMT).

282 ing in epithelial-to-mesenchymal transition (EMT).

283 ance, and epithelial-mesenchymal transition (EMT).

284 ivates epithelial to mesenchymal transition (EMT).

285 ia via epithelial-to-mesenchymal transition (EMT).

286 inducing epithelial-mesenchymal transition (EMT).

287 pathogenic epithelial-mesenchyme transition (EMT).

288 partial epithelial-mesenchymal transitions (EMT).

289 Epithelial-to-mesenchymal transitions (EMTs) are phenotypic plasticity processes that confer mi

290 show how these signals coordinately trigger EMTs and integrate them with broader pathophysiological

291 G3BP2 to enter the nucleus, thus triggering EMT and invasion.

292 PyMT) model, in which tumor cells undergoing EMT would irreversibly switch their fluorescent marker f

293 to forecasting the fate of cells undergoing EMT.

294 Using EMT signature-derived RDIs and data from cell lines repr

295 We have employed varying EMT models of murine breast cancer cells to identify the

296 gnaling in epithelial breast tumor cells via EMT cell-induced production and secretion of VEGF-C.

297 ctive of this study was to determine whether EMT and stemness characteristics induced by TGF-beta mig

298 novel and conserved paracrine means by which EMT cells enhance metastasis, and provides potential tar

299 The mechanisms by which EMT modulators contribute to leukemia pathogenesis, howe

300 exhibited a spectrum of EMT phenotypes, with EMT-related genes concomitantly expressed with the activ