ライフサイエンスコーパス: mammary epithelial cell

1 vesicles and regulates zinc export from the mammary epithelial cell.

2 motes stemness traits and chemoresistance in mammary epithelial cells.

3 program of genes involved in cell growth in mammary epithelial cells.

4 tivities, however, promote transformation of mammary epithelial cells.

5 n breast cancer cell lines, but not in human mammary epithelial cells.

6 2 and zinc transport is tightly regulated in mammary epithelial cells.

7 t that result from abnormal proliferation of mammary epithelial cells.

8 d reduction of Elf5 in miR-193b-null primary mammary epithelial cells.

9 acquisition of stem cell phenotypes in human mammary epithelial cells.

10 ciated microRNAs (SA-miRNAs) in normal human mammary epithelial cells.

11 uent epithelial-to-mesenchymal transition in mammary epithelial cells.

12 ution transplantation experiments of primary mammary epithelial cells.

13 ty in breast cancer cells relative to normal mammary epithelial cells.

14 eded acinus formation in immortalized normal mammary epithelial cells.

15 cell polarity and mesenchymal phenotypes in mammary epithelial cells.

16 liferation in ERBB2-transfected human normal mammary epithelial cells.

17 f ErbB receptor signal transduction in human mammary epithelial cells.

18 sformation to ErbB2-positive, Pak1-deficient mammary epithelial cells.

19 lating signaling by the ErbB2 oncoprotein in mammary epithelial cells.

20 ial role for srGAP3 as a tumor suppressor in mammary epithelial cells.

21 e complex in response to ErbB2 activation in mammary epithelial cells.

22 spontaneous metastasis in transformed human mammary epithelial cells.

23 /beta-catenin and Hgf/Met signaling in mouse mammary epithelial cells.

24 immortal but nontransformed human and mouse mammary epithelial cells.

25 tion of either mTOR or RPTOR triggers EMT in mammary epithelial cells.

26 ctor-3 (GRHL3) in non-transformed basal-like mammary epithelial cells.

27 east cancer cell model and in nontransformed mammary epithelial cells.

28 naling to control branching morphogenesis of mammary epithelial cells.

29 c-Abl to trigger p73-dependent apoptosis in mammary epithelial cells.

30 ssion increased Akt phosphorylation in human mammary epithelial cells.

31 nf12 allele due to nonrandom maternal XCI in mammary epithelial cells.

32 Slug or Sox9 blocks MaSC activity in primary mammary epithelial cells.

33 ge breast cancer cell line and primary human mammary epithelial cells.

34 tiation of MDA-MB-468 breast cancer and HC11 mammary epithelial cells.

35 .5 muM), while not cytotoxic to prostate and mammary epithelial cells.

36 nal upregulation of Twist1 along with EMT in mammary epithelial cells.

37 breast cancer cells without affecting normal mammary epithelial cells.

38 mmaH2AX foci in non-transformed MCF10A human mammary epithelial cells.

39 invasive properties to ErbB2-positive human mammary epithelial cells.

40 promotes cellular energy production in human mammary epithelial cells.

41 helial transition (MET) in mesenchymal human mammary epithelial cells.

42 icity and heterogeneity of transformed human mammary epithelial cells.

43 promoting malignant transformation of human mammary epithelial cells.

44 nd enabled oncogenic transformation of human mammary epithelial cells.

45 ical role of a novel SENP7 isoform SENP7S in mammary epithelial cells.

46 11A has an important role in TNBC and normal mammary epithelial cells.

47 anscriptional repressor that is expressed in mammary epithelial cells.

48 RAIL protein levels in human breast milk and mammary epithelial cells.

49 e but did not affect the viability of normal mammary epithelial cells.

50 ndependent role of Lrp5 in glucose uptake in mammary epithelial cells.

51 eta1-induced epithelial dedifferentiation of mammary epithelial cells.

52 n three-dimensional culture utilizing MCF10A mammary epithelial cells, acini form due to integrin-dep

53 Basal-like nonmalignant mammary epithelial cells also display an altered integri

54 Here, we show that CPEB1-depleted mammary epithelial cells alter their gene expression pro

55 strum contains high levels of PTX3, and that mammary epithelial cell and CD11b(+) milk cells constitu

56 hree-dimensional epithelial morphogenesis of mammary epithelial cells and as a regulator of ErbB2-med

57 GR has been reported to inhibit apoptosis in mammary epithelial cells and breast cancer cells by incr

58 yrosine kinase receptor ErbB2/HER2 in normal mammary epithelial cells and breast cancer cells.

59 -recombined Grp78 floxed alleles in isolated mammary epithelial cells and displayed phenotypes compar

60 ing telomere crisis in human fibroblasts and mammary epithelial cells and document the role of p53 an

61 SIM2s is highly expressed in mammary epithelial cells and downregulated in human brea

62 both the inducible FGFR1 construct in mouse mammary epithelial cells and endogenous FGFR in the trip

63 of primary human BRCA1(+/+) and BRCA1(mut/+) mammary epithelial cells and fibroblasts.

64 by the mis-coordination of the cell cycle in mammary epithelial cells and heterozygote mice spontaneo

65 llular S. aureus as demonstrated in cultured mammary epithelial cells and in a mouse model of staphyl

66 ignals that induce the EMT in nontransformed mammary epithelial cells and in ZR75.1 breast cancer cel

67 T3 to induce a TWIST1-dependent EMT in human mammary epithelial cells and increases breast and bladde

68 that Bnc1 regulates epithelial plasticity of mammary epithelial cells and influences outcome of TGF-b

69 pression is essential for tumor formation by mammary epithelial cells and kidney cells engineered to

70 se cell types was compared with normal human mammary epithelial cells and LNCaP prostate cancer cells

71 Using a combination of experiments with mammary epithelial cells and mathematical modeling, we f

72 Using primary human mammary epithelial cells and monocyte/macrophage cell li

73 However, mammary epithelial cells and mouse tissues knock-out for

74 ib) reversed EMT in mesenchymal normal human mammary epithelial cells and murine BCSCs attenuating se

75 m cell-like populations from non-tumorigenic mammary epithelial cells and non-aggressive breast cance

76 nergistically suppressed the growth of human mammary epithelial cells and revealed a strong, nonlinea

77 that MMTV Env expression transformed normal mammary epithelial cells and that Src kinases were impor

78 lts suggest that pathways controlling p27(+) mammary epithelial cells and the numbers of these cells

79 cation and its consequences in untransformed mammary epithelial cells and tissues.

80 silencing was sufficient to transform normal mammary epithelial cells and to enhance sensitivity to P

81 ate that the repopulating capacity in normal mammary epithelial cells and tumorigenic capacity in TNB

82 udy, we utilized nontransformed human MCF10A mammary epithelial cells and two genetic mouse models [H

83 in vitro (in mouse embryonic fibroblasts and mammary epithelial cells) and in vivo (in mammary outgro

84 UD31 as a MYC-synthetic lethal gene in human mammary epithelial cells, and demonstrate that BUD31 is

85 PIK3R1 knockdown transforms human mammary epithelial cells, and genetic ablation of Pik3r1

86 Overexpression of EMSY in hTERT-immortalized mammary epithelial cells, and in breast and ovarian carc

87 p in the maintenance of genetic stability of mammary epithelial cells, and indicates a new function o

88 is required for efficient transformation of mammary epithelial cells, and suggest new therapeutic st

89 d epithelial-mesenchymal transition (EMT) in mammary epithelial cells, and that SCCA1 silencing in br

90 tumor formation by otherwise nontransformed mammary epithelial cells, and that the initiation of epi

91 receptors are stabilized in Brca1-deficient mammary epithelial cells, and treating with anti-progest

92 ECM-detached mammary epithelial cells are able to rapidly activate au

93 ing Lgr5-EGFP-IRES-CreERT2, to demonstrate a mammary epithelial cell-autonomous requirement of CBL an

94 With knockdown of SENP7S in mammary epithelial cells, Axin1-beta-catenin interaction

95 In transformed human mammary epithelial cells BCL-XL favours full activation

96 exogenous transgenic expression of Runx2 in mammary epithelial cells blocked milk production, sugges

97 Do all mammary epithelial cells both give and take instructions

98 entiation state is common in BRCA1-deficient mammary epithelial cells, but the underlying mechanism i

99 cancer and is required for transformation of mammary epithelial cells by ErbB2.

100 iation, progression, and metastasis in human mammary epithelial cells by increasing the population of

101 further that Erk1/2 is activated in primary mammary epithelial cells by Shh-ligand and that this act

102 a permissive role in TGF-beta-induced EMT in mammary epithelial cells by stimulating SNAI1 expression

103 Hsf1 is indispensable for transformation of mammary epithelial cells by the Her2 oncogene.

104 Here we show that restricting the EMT of mammary epithelial cells by transcription factor Ovol2 i

105 abilizes p53, a Smad partner in premalignant mammary epithelial cells, by downregulating 14-3-3sigma,

106 crochannels based matrix platform to culture mammary epithelial cell clusters in ECMs of tunable stif

107 in the AEBP1(TG) mammary epithelium and HC11 mammary epithelial cells co-cultured with AEBP1(TG) peri

108 rred a significant growth advantage in human mammary epithelial cells, confirming the oncogenic poten

109 alizes to discrete cytoplasmic foci in mouse mammary epithelial cells, consistent with the formation

110 Here we show that normal mammary epithelial cells consume glutamine, but do not s

111 proteins that maintain the growth of starved mammary epithelial cells contingent upon epithelial cell

112 tified the anisotropic stresses generated by mammary epithelial cells cultured within 3D aggregates,

113 with mRNA-Seq data from nontransformed human mammary epithelial cell cultures plus the Illumina Body

114 In mouse mammary epithelial cells, cytoplasmic polyadenylation el

115 cture-function analyses of SgK269 in MCF-10A mammary epithelial cells demonstrated a critical role fo

116 ssion of antioxidant enzymes in nonmalignant mammary epithelial cells detached from ECM resulted in A

117 equired for ErbB4 ICD-mediated inhibition of mammary epithelial cell differentiation in a three-dimen

118 -mediated activation of LAP1 participates in mammary epithelial cell differentiation.

119 LAP1 operate in a common pathway to promote mammary epithelial cell differentiation.

120 transcription factors and a key regulator of mammary epithelial cell differentiation.

121 nscription factor C/EBPbeta are required for mammary epithelial cell differentiation; however, the pa

122 Furthermore, mammary epithelial cell-directed expression of an activa

123 ying the production and expulsion of milk by mammary epithelial cells during lactation remains largel

124 Mammary epithelial cells engage regulatory pathways that

125 ty to interfere with TGF-beta-induced EMT in mammary epithelial cells (EpH4) expressing oncogenic Ras

126 deed, depletion of endogenous LRIG1 in human mammary epithelial cells expands the stem cell populatio

127 ween breast cancer risk and the frequency of mammary epithelial cells expressing p27, estrogen recept

128 These mammary epithelial cells expressing Smarcd3/Baf60c had u

129 abundance data collected in a panel of human mammary epithelial cells expressing varying levels of EG

130 Klf4 and c-Myc) into MCF-10A nontumorigenic mammary epithelial cells, followed by partial differenti

131 ification was also observed in primary human mammary epithelial cells following exposure to radiation

132 We now report that BTG2 protects human mammary epithelial cells from oxidative stress due to hy

133 GFR)-mediated cell signaling is critical for mammary epithelial cell growth and survival; however, ta

134 The mouse mammary epithelial cell hierarchy contains both multipot

135 We used an isogenic human mammary epithelial cell (HMEC) culture model, derived fr

136 screen for novel oncogenes that drive human mammary epithelial cell (HMEC) transformation.

137 utively active CCND1/CDK2 complexes in human mammary epithelial cell (HMEC) transformation.

138 Primary human mammary epithelial cells (HMEC's) were labeled with 35S-

139 OD was not detectable in non-malignant human mammary epithelial cells (HMEC) cultured in conventional

140 antification of ERK phosphorylation in human mammary epithelial cells (HMEC) was demonstrated from as

141 nstrate that reducing mtDNA content in human mammary epithelial cells (hMECs) activates Calcineurin (

142 Here we show that human mammary epithelial cells (HMECs) from BRCA1-mutation car

143 HACE1 downregulation in normal human mammary epithelial cells (HMECs) results in the accumula

144 length and truncated ERBB2 isoforms in human mammary epithelial cells (HMECs), including HMEC and MCF

145 cancer cell lines compared with normal human mammary epithelial cells (HMECs).

146 sal of EMT in snail-transduced primary human mammary epithelial cells (HMECs).

147 lower hsa-miR-125b levels than normal human mammary epithelial cells (HMECs).

148 endent growth of partially transformed human mammary epithelial cells (HMECs).

149 in the transformation of immortalized human mammary epithelial cells (HMECs).

150 r initiation in models of immortalized human mammary epithelial cells (HMECs).

151 growth in a derivative of immortalized human mammary epithelial cells (HMLE).

152 ge-independent colony growth of human MCF10A mammary epithelial cells, identifying S71A/S81A and T343

153 Human mammary epithelial cells immortalized through TERT expre

154 profiles of polarized and disorganized human mammary epithelial cells in a physiologically relevant t

155 sicular zinc accumulation and secretion from mammary epithelial cells in a transient manner.

156 induce EMT in normal and immortalized human mammary epithelial cells in an apparent positive feedbac

157 tional loss of full-length BRCA1 targeted to mammary epithelial cells in association with germline TP

158 comparable or lower toxicity to normal human mammary epithelial cells in comparison with 1.

159 glucose uptake regulates the growth rate of mammary epithelial cells in culture.

160 ssue-specific disruption of the casr gene in mammary epithelial cells in MMTV-PymT mice reduced tumor

161 at can promote the proliferation of cultured mammary epithelial cells in response to cyclic or static

162 or PTPalpha in the regulation of motility of mammary epithelial cells in response to ErbB2 activation

163 beta1-integrin gene from primary cultures of mammary epithelial cells in situ, using CreER.

164 r-, progesterone receptor-, or ki67-positive mammary epithelial cells in the transgenic mice at the l

165 pared to the MCF10A model of non-tumorigenic mammary epithelial cells in three dimensional (3D) overl

166 e small intestine, while ILDR1 in EpH4 mouse mammary epithelial cells in vitro was shown to recruit t

167 eration of hormone receptor-positive (HR(+)) mammary epithelial cells in vivo.

168 , and SW48 colorectal cancer cells and human mammary epithelial cells in which a single copy of mutan

169 le mice are fertile but contain disorganized mammary epithelial cells, in which zonal occludens-1 and

170 RUNX1 loss in ER(+) mammary epithelial cells increases beta-catenin, deregul

171 Overexpression of GPR161 in human mammary epithelial cells increases cell proliferation, m

172 We find that, in normal mammary epithelial cells, increasing ECM stiffness alone

173 Gene expression studies with normal mammary epithelial cells indicated that rexinoids modula

174 sion of Smarcd3/Baf60c in immortalized human mammary epithelial cells induced an EMT.

175 inactivation of murine Rb and p53 in diverse mammary epithelial cells induced claudin-low-like TNBC w

176 dings, we found that NAMPT overexpression in mammary epithelial cells induced epithelial-to-mesenchym

177 ere we report that LMW-E expression in human mammary epithelial cells induces an epithelial-to-mesenc

178 e report that homozygous deletion of PTEN in mammary epithelial cells induces tubulin-based microtent

179 activation of RORalpha in nonmalignant human mammary epithelial cells inhibited SEMA3F transcription

180 During late embryogenesis, mammary epithelial cells initiate migration programs tha

181 yer in the response to Wnt3a-type ligands in mammary epithelial cells; instead, Lrp5 is required for

182 ut the role of XBP1 in cancer progression in mammary epithelial cells is largely unknown.

183 In mammary epithelial cells, JARID1B loss diminished the ex

184 ilk somatic cells (SC), laser microdissected mammary epithelial cells (LCMEC), milk fat globules (MFG

185 ShRNA-mediated attenuation of CCN6 in human mammary epithelial cells led to BMP4 upregulation as a m

186 ntradictory reports on an immortalized human mammary epithelial cell line (HMLE) that underwent EMT.

187 A non-tumorigenic normal mammary epithelial cell line (MCF-10A) was markedly more

188 d Hs68 diploid fibroblasts, the H184B5F5/M10 mammary epithelial cell line, HT1080 fibrosarcoma cells,

189 is directly regulated by miR-424 in multiple mammary epithelial cell lines and observe the loss of MG

190 s in estrogen receptor positive and negative mammary epithelial cell lines demonstrate a role for Agr

191 nsient expression of FOXC1 in nontransformed mammary epithelial cell lines resulted in significantly

192 rate BRCA2 conditional non-transformed human mammary epithelial cell lines using CRISPR-Cas9.

193 trength between metastatic and nonmetastatic mammary epithelial cell lines, which occur over concentr

194 models compared to non-metastatic and normal mammary epithelial cell lines.

195 and activation patterns in a panel of human mammary epithelial cells lines with known HER expression

196 of focal adhesion kinase (FAK) in embryonic mammary epithelial cells (MaEC) decreases luminal progen

197 We show that purified normal human basal mammary epithelial cells maintain low levels of ROS prim

198 Viability analysis of normal mammary epithelial cells (MCF-12A) under oxygen gradient

199 r and embryonic stem cells (ESCs) to adopt a mammary epithelial cell (MEC) fate.

200 o effects of AZD4547 on mammary development, mammary epithelial cell (MEC) populations, and oncogenic

201 embryonic stem cell (ESC) self-renewal, and mammary epithelial cell (MEC) reprogramming to induced p

202 of humans and mice are comprised of two main mammary epithelial cell (MEC) subtypes: a surrounding la

203 expression of cyclin D1 is believed to endow mammary epithelial cells (MEC) with a proliferative adva

204 -kinase (PI3K), have been shown to transform mammary epithelial cells (MEC).

205 tion in Cbl-b-null, Cbl-c-null primary mouse mammary epithelial cells (MECs) (Cbl triple-deficiency)

206 ulating the motility of normal and malignant mammary epithelial cells (MECs) and elicits robust compe

207 Characterising the hierarchy of mammary epithelial cells (MECs) and how they are regulat

208 roliferating vs. functionally differentiated mammary epithelial cells (MECs) and to study their corre

209 val, and promotes the malignant phenotype of mammary epithelial cells (MECs) by increasing alpha5 int

210 f MESCs, the inactivation of ATM by R175H in mammary epithelial cells (MECs) could contribute to the

211 is expressed in all subpopulations of murine mammary epithelial cells (MECs) except the secretory alv

212 ErbB3 is required in luminal mammary epithelial cells (MECs) for growth and survival.

213 Profiling of RNA from mouse mammary epithelial cells (MECs) isolated on pregnancy da

214 Mechanisms regulating the transition of mammary epithelial cells (MECs) to mammary stem cells (M

215 entrally involved in integrating signals for mammary epithelial cells (MECs) to navigate the collagen

216 ctin promotes lactational differentiation of mammary epithelial cells (MECs) via its cognate receptor

217 Pretreatment of mammary epithelial cells (MECs) with the phosphatidylino

218 nd receptors are recruited to the surface of mammary epithelial cells (MECs), and the vesicle transpo

219 d by widespread cell death in milk-producing mammary epithelial cells (MECs).

220 expressed in breast cancer cells but not in mammary epithelial cells (MECs).

221 ZnT2-overexpression activates cell death in mammary epithelial cells (MECs).

222 static breast cancer cells but not in normal mammary epithelial cells, miR-218 enhances Wnt activity

223 at globules (MFG) and antibody-captured milk mammary epithelial cells (mMEC) to analyze the bovine ma

224 ed an in vitro assay, in which primary mouse mammary epithelial cells (mMECs) progressed from lumenal

225 onstitution of BRCA1 in Brca1-deficent mouse mammary epithelial cells (MMECs) promoted Foxa1 expressi

226 se genome editing to study 8p deletions in a mammary epithelial cell model and show that 8p loss of h

227 ine phosphatases (PTPs) in three-dimensional mammary epithelial cell morphogenesis and ERBB2 signalin

228 ematopoietic stem cells and the expansion of mammary epithelial cells, neural progenitors and fibrobl

229 ow either cytotoxicity on noncancerous human mammary epithelial cells nor toxic effects in vivo, sugg

230 Here, by depleting mammary epithelial cells of RUNX1 in vivo and in vitro,

231 n, demonstrated by defective dye coupling in mammary epithelial cells of Tg mice.

232 cell differentiation, is markedly reduced in mammary epithelial cells of transgenic mice.

233 conditional expression of ERalpha in luminal mammary epithelial cells on the mes background facilitat

234 ediator of beta-catenin signaling and normal mammary epithelial cell physiology.

235 The latter-also termed parity-identified mammary epithelial cells (PI-MECs)-are marked by beta-ga

236 is essential for tight-junction assembly and mammary epithelial cell polarity.

237 Here, we identify a quiescent mammary epithelial cell population expressing high level

238 OH)22, while essentially not toxic to normal mammary epithelial cells, possesses intrinsic inhibitory

239 one provides effective growth suppression of mammary epithelial cells, potentially dissociating syste

240 We found that expression of Twist1 in human mammary epithelial cells potently promoted angiogenesis.

241 on and transcriptional activity that induces mammary epithelial cell proliferation and breast cancer

242 Efatutazone treatment reduced rates of mammary epithelial cell proliferation and development of

243 Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbr

244 s decreased serum estrogen level and reduced mammary epithelial cell proliferation in early puberty.

245 Elevated Zpo2 levels increase mammary epithelial cell proliferation.

246 Knockdown of miR-205 in mammary epithelial cells promoted epithelial-mesenchymal

247 Here, we show that loss of Par3 in mammary epithelial cells promotes apoptosis, and that on

248 eal a novel function for Runx2 in regulating mammary epithelial cell regenerative potential, possibly

249 e dimensions, whereas nontransformed MCF-10A mammary epithelial cells require much wider micropattern

250 stimulation by FGF2, and Ptprb knockdown in mammary epithelial cells resulted in a higher level of f

251 During lactation, mammary epithelial cells secrete huge amounts of milk fr

252 In immortalized MCF-10A mammary epithelial cells, SgK269 promoted transition to

253 ErbB3 loss in mammary epithelial cells shifted gene expression pattern

254 BRCA1-deficient mouse primary mammary epithelial cells show low expression of Nrf2-reg

255 we found that, in Pttg1-mutant females, the mammary epithelial cells showed increased proliferation

256 Silencing RORalpha in mammary epithelial cells significantly enhanced cell pro

257 resulted in gene expression changes in human mammary epithelial cells similar to that of claudin-low

258 Here, we used purified primary mammary epithelial cells stimulated with fibroblast grow

259 generated a large collection of normal human mammary epithelial cell strains from women ages 16 to 91

260 th breast malignant cell subtypes and normal mammary epithelial cell subpopulations and suggest thera

261 ial-to-mesenchymal transition (EMT) of human mammary epithelial cells, suggesting that LRIG1 expressi

262 In a human mammary epithelial cell system that recapitulates early

263 pproach to engineer ducts composed of normal mammary epithelial cells that contained a single tumor c

264 splice variant of HER2 (Delta-HER2) in human mammary epithelial cells that evokes aggressive breast c

265 r and differentiation maintenance process in mammary epithelial cells that may contribute to sporadic

266 ependent apoptosis in MCF10A cells and human mammary epithelial cells that overexpress the MYC oncoge

267 ress response in mortal nontumorigenic human mammary epithelial cells that subsequently induces desmo

268 We have found that human mammary epithelial cells that undergo an epithelial-to-m

269 e oxygen species (ROS) occur in ECM-detached mammary epithelial cells, threatening cell viability by

270 at rexinoids activate a lipogenic program in mammary epithelial cells through a retinoid X receptor/P

271 ition or gene silencing of PDGFRs sensitizes mammary epithelial cells to chemotherapeutic agents in v

272 restores the ability of C/EBPbeta-deficient mammary epithelial cells to differentiate and does so in

273 lation is critical in transition from normal mammary epithelial cells to endocrine-responsive ESR1-po

274 w that deregulation of cyclin E causes human mammary epithelial cells to enter into mitosis with shor

275 diates the ubiquitination of ErbB3 in normal mammary epithelial cells to facilitate receptor degradat

276 ANCE Here, we use an in vitro model of human mammary epithelial cell transformation to assess how mal

277 to be one key effector of IKKepsilon-induced mammary epithelial cell transformation.

278 of activation in an in vitro model of human mammary epithelial cell transformation.

279 In contrast, Sharpin(cpdm) mammary epithelial cells transplanted in vivo into wild-

280 in cultured breast tumor and non-tumorigenic mammary epithelial cells, TRIM29 is up-regulated in resp

281 ) properties, by culturing transformed human mammary epithelial cells under normoxic and hypoxic cond

282 chanistically, MTDH supports the survival of mammary epithelial cells under oncogenic/stress conditio

283 when detached from the matrix, untransformed mammary epithelial cells undergo metabolic reprogramming

284 gnalling is decreased, matrix-attached human mammary epithelial cells upregulate and internalize beta

285 s primarily associated with supporting human mammary epithelial cell viability, and, moreover, preven

286 the antioxidant enzyme EcSOD in normal human mammary epithelial cells was not recognized until recent

287 Delta-HER2 overexpression in mammary epithelial cells was sufficient to reduce apopto

288 system and other approaches to culture human mammary epithelial cells, we find that centrosome amplif

289 Using MCF-10A mammary epithelial cells, we show that exposure to exoge

290 cooperating with HER2/neu to fully transform mammary epithelial cells, we used an insertional mutagen

291 In primary mammary epithelial cells, we used lentivirus-mediated kn

292 A closer examination showed that their mammary epithelial cells were not able to maintain funct

293 TNBC cells, but not nonmalignant mammary epithelial cells, were dependent on PIM1 for pro

294 of MCF-7 breast cancer cells versus MCF-10A mammary epithelial cells, when subjected to individual a

295 w that beta1-integrins promote cell cycle in mammary epithelial cells, whereas beta3-integrins are in

296 esenchymal transition-like changes in normal mammary epithelial cells, whereas Runx2 deletion in basa

297 Treatment of non-tumorigenic mammary epithelial cells with exosomes derived from aggr

298 and DOCK5 extends to non-transformed MCF10A mammary epithelial cells, with DOCK5 'dialing-up' and GI

299 genic mice (NRL-PRL) that overexpress PRL in mammary epithelial cells, with wild-type, heterozygous,

300 nges over time, here, we study the motion of mammary epithelial cells within engineered monolayers, i