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 promotes cellular energy production in human mammary epithelial cells.

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

4 icity and heterogeneity of transformed human mammary epithelial cells.

5 ducts and enhanced TGFbeta1 activity within mammary epithelial cells.

6 promoting malignant transformation of human mammary epithelial cells.

7 nd enabled oncogenic transformation of human mammary epithelial cells.

8 11A has an important role in TNBC and normal mammary epithelial cells.

9 anscriptional repressor that is expressed in mammary epithelial cells.

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

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

12 eta1-induced epithelial dedifferentiation of mammary epithelial cells.

13 motes stemness traits and chemoresistance in mammary epithelial cells.

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

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

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

17 2 and zinc transport is tightly regulated in mammary epithelial cells.

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

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

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

21 ation at the cortical cytoskeleton in normal mammary epithelial cells.

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

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

24 ution transplantation experiments of primary mammary epithelial cells.

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

26 eded acinus formation in immortalized normal mammary epithelial cells.

27 cell polarity and mesenchymal phenotypes in mammary epithelial cells.

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

29 g-term proliferation of normal and malignant mammary epithelial cells.

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

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

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

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

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

35 spontaneous metastasis in transformed human mammary epithelial cells.

36 immortal but nontransformed human and mouse mammary epithelial cells.

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

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

39 naling to control branching morphogenesis of mammary epithelial cells.

40 roliferation and tumorigenesis in BRCA1(-/-) mammary epithelial cells.

41 rved in OMA1-depleted non-tumorigenic MCF10A mammary epithelial cells.

42 east cancer cells, but not in nontumorigenic mammary epithelial cells.

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

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

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

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

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

48 coplasma infection was investigated in mouse mammary epithelial cells.

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

50 e PAK4 overexpression in untransformed human mammary epithelial cells abrogates H-RAS-V12-induced sen

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

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

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

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

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

56 miR-489, we sorted different populations of mammary epithelial cells and determined that miR-489 was

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

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

59 nal profiling of normal ER(+) mature luminal mammary epithelial cells and ER(+) breast tumors reveale

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

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

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

63 pha (ER-alpha) forms a regulatory network in mammary epithelial cells and in breast cancer with the t

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

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

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

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

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

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

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

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

72 x perturbation experiment with primary human mammary epithelial cells and multiplex cryopreserved tum

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

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

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

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

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

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

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

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

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

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

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

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

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

86 r their influence on the function of primary mammary epithelial cells, and tumor epithelial cells usi

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

88 tumors initiated from different precancerous mammary epithelial cells are distinct.

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

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

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

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

93 Bovine mammary epithelial cells (bMECs) are the main cells of t

94 Do all mammary epithelial cells both give and take instructions

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

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

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

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

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

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

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

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

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

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

105 logy observed in mammary epithelium in vivo, mammary epithelial cells cultured on soft microenvironme

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

107 In mouse mammary epithelial cells, cytoplasmic polyadenylation el

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

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

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

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

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

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

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

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

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

117 Mammary epithelial cells engage regulatory pathways that

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

119 Breast and mammary epithelial cells experience different local envi

120 Finally, mammary epithelial cell exposure to SAM milk pellets sho

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

122 These mammary epithelial cells expressing Smarcd3/Baf60c had u

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

124 and redirect cancer cells to adopt a normal mammary epithelial cell fate in vivo.

125 In primary mammary epithelial cells, fermentative glycolysis, and i

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

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

128 optotic roles of P. zopfii GT-II in cultured mammary epithelial cells (from cattle and mice) and muri

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

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

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

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

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

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

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

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

137 D) colony organization of premalignant human mammary epithelial cells (HMECs) is one of the indices o

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

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

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

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

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

143 abolomics to analyze senescent primary human mammary epithelial cells (HMECs).

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

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

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

147 Human mammary epithelial cells immortalized through TERT expre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 example, transcriptome analysis of purified mammary epithelial cells isolated from bigenic NIC-PRMT1

174 In mammary epithelial cells, JARID1B loss diminished the ex

175 utilizes a premalignant phenotype of normal mammary epithelial cells lacking PTEN.

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

177 ation and localization was altered in STM KO mammary epithelial cells, leading to decreased protein s

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

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

180 in cultured cells was studied using a human mammary epithelial cell line that expresses SULT1A3 at l

181 and the cis-regulatory networks of two human mammary epithelial cell lines (184A1 and MCF10A) are inv

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

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

184 Furthermore, mammary epithelial cell lines were exposed to milk pelle

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

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

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

188 In mouse mammary epithelial cells, loss of stathmin compromised t

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

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

191 mation (~1% projected area strain) in normal mammary epithelial cells (MCF-10A cells) was sufficient

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

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

194 ion; ZnT2-null mice have profound defects in mammary epithelial cell (MEC) polarity and secretion, re

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

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

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

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

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

200 -II (but not GT-I) invaded bovine and murine mammary epithelial cells (MECs) and induced apoptosis, a

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

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

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

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

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

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

207 series of cellular and molecular changes in mammary epithelial cells (MECs) of female adults.

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

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

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

211 feasible with conventional static hydrogels, mammary epithelial cells (MECs) were cultured on methacr

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

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

214 In mammary epithelial cells (MECs), BRCA1 interacts with mu

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

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

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

218 In normal luminal mammary epithelial cells, miR-223 acted cell autonomousl

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

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

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

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

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

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

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

226 R-loops and DNA damage were also detected in mammary epithelial cells of mice treated with BP-3 and P

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

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

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

230 and survival of E-cadherin-deficient murine mammary epithelial cells on stiff matrices like fibrilla

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

232 Here, we show that dispersed mammary epithelial cells organize into arrested, fractal

233 Here we examine the role of vinculin in mammary epithelial cell phenotype.

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

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

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

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

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

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

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

241 in apicobasal polarity defects and increased mammary epithelial cell proliferation associated with hy

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

243 Elevated Zpo2 levels increase mammary epithelial cell proliferation.

244 density-induced increase in Akt activity and mammary epithelial cell proliferation.

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

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

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

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

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

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

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

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

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

254 Silencing RORalpha in mammary epithelial cells significantly enhanced cell pro

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

256 letion of macrophages in obese mice enhanced mammary epithelial cell stem/progenitor activity, elevat

257 Recent experimental studies on mouse HC11 mammary epithelial cells stimulated by ligand Neuregulin

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

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

260 In a human mammary epithelial cell system that recapitulates early

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

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

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

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

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

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

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

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

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

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

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

272 y co-printing cancer cells along with normal mammary epithelial cells to generate chimeric organoids.

273 RNP E1 knockdown significantly shifts normal mammary epithelial cells to mesenchymal BCSCs in vitro a

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

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

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

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

278 etabolic programs in cancer cells, influence mammary epithelial cell tumorigenicity and aggressivenes

279 er resolution representation of the multiple mammary epithelial cell types in the organoids, and demo

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

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

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

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

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

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

286 he density-dependent proliferation of murine mammary epithelial cells, we developed a fluorescence-ac

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

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

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

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

291 V-miR-489 mice that overexpressed miR-489 in mammary epithelial cells were developed and these mice e

292 ddition, we found that normal human lung and mammary epithelial cells were less sensitive to acute DH

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

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

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

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

297 This dramatic impact was also observed in mammary epithelial cells with constitutively high levels

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

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

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