ライフサイエンスコーパス: MCF-7 cell

1 distribution was shown for the EI output of MCF-7 cells.

2 equent interactions than are observed in the MCF-7 cells.

3 K signaling to support junctional tension in MCF-7 cells.

4 actor)-mediated activation of ERK and AKT in MCF-7 cells.

5 ading to increased migration and invasion in MCF-7 cells.

6 s candidates for regulation were examined in MCF-7 cells.

7 level is low but inducible by epirubicin in MCF-7 cells.

8 ing sequence and expressed these proteins in MCF-7 cells.

9 late the proliferation of estrogen-sensitive MCF-7 cells.

10 binding of WA to Cys(303) of beta-tubulin in MCF-7 cells.

11 blockade) and depolymerization of tubulin in MCF-7 cells.

12 moter also occurs in human Hep3B, HepG2, and MCF-7 cells.

13 s used to specifically recognize and capture MCF-7 cells.

14 ntracellular ATP and GTP imaging in cultured MCF-7 cells.

15 gligible binding to alpha(v)beta(3)-negative MCF-7 cells.

16 by RNAi further promotes VEGF expression in MCF-7 cells.

17 to characterize estrogen responsive genes in MCF-7 cells.

18 dance change is observed for less-metastasis MCF-7 cells.

19 ably reduced, PRNP and ERLEC1 mRNA levels in MCF-7 cells.

20 dynamics of individual microtubules in live MCF-7 cells.

21 r RBP SRSF5 affects splicing of Mcl-1 in the MCF-7 cells.

22 produced and used for uptake experiments in MCF-7 cells.

23 were detected in tamoxifen-resistant (TAM-R) MCF-7 cells.

24 intracellular secretory vesicles in HC11 and MCF-7 cells.

25 phosphorylation and nuclear accumulation in MCF-7 cells.

26 ac1 abolished tRA-induced phosphorylation in MCF-7 cells.

27 ively), the tRA-stimulated NIS expression in MCF-7 cells.

28 nd p38beta for the full expression of NIS in MCF-7 cells.

29 e-Guerin levels in mammary epithelial cancer MCF-7 cells.

30 tions of PERK inhibitor compared to parental MCF-7 cells.

31 ionally interact at target gene promoters in MCF-7 cells.

32 erentially induce apoptosis over necrosis in MCF-7 cells.

33 duce G(0)/G(1) growth arrest of asynchronous MCF-7 cells.

34 dependently induce an MDR1/P-gp phenotype in MCF-7 cells.

35 regulated by 4-OHT via endogenous ERbeta in MCF-7 cells.

36 transcriptional activation and expression in MCF-7 cells.

37 OHT(R) cells and increased in TIMP3-depleted MCF-7 cells.

38 Cs and no or weak cell-cell interactions for MCF-7 cells.

39 the binding of key transcription factors in MCF-7 cells.

40 in rabbit reticulocyte lysate, bacteria, and MCF-7 cells.

41 vealed promising anticancer activity against MCF-7 cells.

42 K1, but not SphK2, increased S1P export from MCF-7 cells.

43 ptional activity and protein accumulation in MCF-7 cells.

44 in MCF-7-T-bet cells and in insulin-treated MCF-7 cells.

45 YPIB1 were both inducible by dioxin in human MCF-7 cells.

46 as compared to parental, tamoxifen-sensitive MCF-7 cells.

47 n estrogen receptor alpha (ERalpha)-positive MCF-7 cells.

48 ed rapid release of S1P and dihydro-S1P from MCF-7 cells.

49 F promoter in a P-TEFb-independent manner in MCF-7 cells.

50 observation that miR-19 levels are higher in MCF-7 cells.

51 e interaction of Mt-HSA NCs/PGE surface with MCF-7 cells.

52 ocytes, and modulated DNA damage response in MCF-7 cells.

53 S1P pathway and is normally not expressed in MCF-7 cells.

54 fectively reduced the PRMT5 protein level in MCF-7 cells.

55 on of cell proliferation than fulvestrant in MCF-7 cells.

56 both, or absence of any such protrusions in MCF-7 cells.

57 the genome at near-nucleotide resolution in MCF-7 cells.

58 ntration of 2nM) on electrochemical activity MCF-7 cells.

59 and morphological changes of MDA-MB-231 and MCF-7 cells.

60 tive response in human breast adenocarcinoma MCF-7 cells.

61 activity and thus increased miR-221 level in MCF-7 cells.

62 ntargeted mass-spectroscopy metabolomics for MCF-7 cells.

63 hIP-BIT as being differentially expressed in MCF-7 cells.

64 ha1,2- and alpha1,3 fucose linkages found in MCF-7 cells.

65 currence of open compartments on chr16-22 in MCF-7 cells.

66 1895 protein groups were identified from 100 MCF-7 cells (~10 ng protein content).

67 e peptides and 3069 protein groups from 1000 MCF-7 cells (~100 ng protein content), and 13 367 peptid

68 rnalization at MI=1.0, 79.5% at MI=1.5) than MCF-7 cells (42.4% internalization at MI=1.0, 35.7% at M

69 MCF-7 cells, a human breast adenocarcinoma, were retaine

70 knockdown of p62 by small interfering RNA in MCF-7 cells abrogates Vps34-dependent tumor growth.

71 In MCF-7 cells, ADAM15E was the principal variant inducing

72 creased by 1.60 nmol (61.1 %) in 3.0 x 10(6) MCF-7 cells after 100 nM insulin stimulation.

73 -dose coexposures of human mammary carcinoma MCF-7 cells against polycyclic aromatic hydrocarbons (PA

74 -UTR negatively regulates gene expression in MCF-7 cells, an effect reversed by deletion of the miR-1

75 d deprivation is significantly attenuated in MCF-7 cells, an ER-positive breast cancer cell line, whe

76 or their actions against tamoxifen-resistant MCF-7 cells and a patient-derived xenograft triple-negat

77 d the dynamics of individual microtubules in MCF-7 cells and delayed the reassembly of depolymerized

78 Both senescence of MCF-7 cells and differentiation of MDA-MB-231 cells were

79 e cellular uptake of the monodisperse CDs in MCF-7 cells and Huh-7 liver cancer cells.

80 r component of ATRA-induced growth arrest of MCF-7 cells and identify S6K as a novel downstream targe

81 n of Trask expression and phosphorylation in MCF-7 cells and in 3T3v-src cells was associated with a

82 05-ERbeta nuclear speckles were also seen in MCF-7 cells and markedly increased in size and number at

83 orce of cancer cells representing malignant (MCF-7 cells and MDA-MB-231 cells) and nonmalignant (MCF-

84 tion of receptor PTPepsilon (RPTPepsilon) in MCF-7 cells and MDA-MB-231 upon PMA, FGF, and serum stim

85 aTC cell lines showed the highest uptake by MCF-7 cells and negligible uptake by the healthy cells (

86 formance for the ultrasensitive detection of MCF-7 cells and quantification of cell surface glycan.

87 ate in MCF-7/MX100 cells but not in parental MCF-7 cells and sensitized the MDR cells to the chemothe

88 TPSF reduces ERalpha protein levels in MCF-7 cells and several other cell lines without alterin

89 shed for complex 5.Let against breast cancer MCF-7 cells and significantly lower activity against gli

90 ignificantly elevated in tamoxifen-resistant MCF-7 cells and T47D cells.

91 ROS formation in MCF-7 cells and three-dimensional (3D) spheroids was pro

92 ression to be basally repressed by Nkx3-1 in MCF-7 cells and TOT treatment appeared to elevate Nkx3-1

93 e deglycoBLM conjugate, bound selectively to MCF-7 cells and were internalized.

94 In MCF-7 cells and xenograft tumors, MnO2 /DVDMS is reduced

95 om 1.5 x 10(2) to 7.5 x 10(6) breast cancer (MCF-7) cells and the limit of detection was calculated a

96 to adenosine 5'-diphosphate or tumor cells (MCF-7 cells) and exhibited a decreased angiogenic potent

97 ty to penetrate the cell membrane in 3T3 and MCF-7 cells, and cationic PNAs were found to be accumula

98 nhances UVC irradiation-induced apoptosis in MCF-7 cells, and causes sensitization to DNA-damaging dr

99 cell growth: it showed IC(5)(0) = 1.0 nM in MCF-7 cells, and it was uniformly active in the whole pa

100 duces endogenous tissue factor expression in MCF-7 cells, and overexpression of miR-19 down-regulates

101 s was dramatically reduced in the Cav-1 null MCF-7 cells, and PIV-5 grown in MCF-7 cells had a reduce

102 n bone marrow, multiple leukemia cell lines, MCF-7 cells, and subjects after GM-CSF treatment but not

103 rogen responsive element (ERE)-luciferase in MCF-7 cells, and Tff1 mRNA in T47D cells.

104 RB inactivation increases IL-6 production in MCF-7 cells appeared to involve fatty acid oxidation (FA

105 The effects of BJ3Z cells on MCF-7 cells are equivalent to those of E(2).

106 A and increased with OTUB1 overexpression in MCF-7 cells, arguing that OTUB1 positively regulates FOX

107 Using MCF-7 cells as a model system, we show that ATRA stimula

108 Using MCF-7 cells as in vitro model for anti-cancer mechanisti

109 tro, disrupted the microtubular structure in MCF-7 cells as visualized by confocal microscopy, and ca

110 ds preferentially to tissue factor 3'-UTR in MCF-7 cells, as compared with MDA-MB-231 cells, consiste

111 Similarly, in MCF-7 cells, BCAR3-induced tyrosine phosphorylation of t

112 ficantly elevate FGF20 protein production in MCF-7 cells, between two- and four-fold.

113 growth in vitro and uterine enlargement and MCF-7 cell breast cancer xenograft growth in vivo were s

114 cited cytosolic Ca(2+) increases not only in MCF-7 cells but also in ER-negative SKBr3 cells.

115 nificant decrease in Mcl-1 protein levels in MCF-7 cells but an increase in JAR cells, respectively,

116 ndependent E(2)-ERalpha-stimulated growth of MCF-7 cells but does not inhibit growth of ER-negative M

117 nse element-dependent luciferase activity in MCF-7 cells but not in MCF-7 stable cells expressing app

118 time-dependent manner in the drug-sensitive MCF-7 cells but not in the resistant counterparts in res

119 Inactive pro-invasive genes in MCF-7 cells but not in U251 cells frequently exhibited a

120 riphosphate receptor mediated in ER-positive MCF-7 cells but transitory and ryanodine receptor mediat

121 on reduced upon genotoxic agent treatment in MCF-7 cells, but remained relatively constant in resista

122 on of ERbeta1 promoted growth suppression in MCF-7 cells, but the anti-proliferative effects of ERbet

123 These TPEs all stimulate growth in MCF-7 cells, but unlike the planar estrogens they block

124 Global transcript profiling of MCF-7 cells by RNA-seq shows that FDI-6 specifically dow

125 nstrated that the ectopic EPSTI1 granted the MCF-7 cells capability of both invasive growth in the br

126 These approaches achieved MCF-7 cell capture from </=10 microL of whole blood with

127 as observed for the viability of HCT 116 and MCF-7 cells challenged with 0.4, 4.0, and 40mug/ml nanoe

128 [Deltaf] and motional resistance DeltaR) of MCF-7 cells compared with those of HMECs mirror the canc

129 MCF-7 cells concentrated in S-phase or G0/G1-phase were

130 de based platform for breast cancer specific MCF-7 cell concentration estimation and their molecular

131 des were exposed to solutions with different MCF-7 cell concentrations and CV technique was used to d

132 and cellular characterization using U937 and MCF-7 cells confirmed that many of these analogues displ

133 A tumor xenograft with Mel-18 knockdown MCF-7 cells consistently showed increased ZEB1 and ZEB2

134 ater) from seven individuals, and (iv) human MCF-7 cells cultured in vitro (Kcell/water).

135 ma hyorhinis-infected human breast carcinoma MCF-7 cell cultures (MCF-7.Hyor), depending on the prope

136 and assays involving microscopy imaging and MCF-7 cells culturing can be performed in 2-3 d.

137 ther, flow cytometry showed that G-1 blocked MCF-7 cell cycle progression at the G(1) phase.

138 Silencing EDI3 in MCF-7 cells decreased this enzymatic activity, increased

139 The IC50 of DHA or EPA in MCF-7 cells decreased when combined with E2 (10 nM) trea

140 Co-immunoprecipitation studies in MCF-7 cells demonstrated a direct interaction between p3

141 injections in mice with human breast cancer MCF-7 cells depleted for SMAR1 showed increased CD44 var

142 Importantly, MCF-7 cell-derived exosomes that are caspase-3-deficient

143 ata and RNA polymerase II ChIA-PET data from MCF-7 cells did not suggest remote effects of the enhanc

144 net-based separation for the isolation of 50 MCF-7 cells directly from whole blood.

145 ited proliferation and promoted apoptosis of MCF-7 cells dose- and time-dependently.

146 ion of ERalpha by RNA interference (RNAi) in MCF-7 cells downregulated FOXM1 expression.

147 s well as in its ability to degrade Her-2 in MCF-7 cells (EC(50) = 14 vs 38 nM).

148 Autocrine activation of STAT3 in MCF-7 cells ectopically expressing OSM-induced cellular

149 Transcriptomes of MCF-7 cells exposed to varying concentrations of represe

150 ell viability and abrogate DSBs sustained by MCF-7 cells following epirubicin, owing to an enhancemen

151 lular lactate production and the capacity of MCF-7 cells for anchorage independent growth in soft aga

152 was transiently overexpressed (~5.4-fold) in MCF-7 cells for whole genome miRNA profiling (miRNA-seq)

153 rphyrazines with EC50 values as low as 5 nM (MCF-7 cells) for the best compound; this activity was se

154 of adherent colon (HT-29) and breast cancer (MCF-7) cells from the interphase through mitosis and the

155 was the most potent extract, particularly in MCF-7 cells (GI(50) 25.2+/-0.2 mug/ml).

156 Additionally, in MCF-7 cells, GPR30 depletion blocked E(2)-induced and G-

157 Cytoplasmic extracts of MCF-7 cells grown under hypoxia (1% oxygen) recapitulate

158 was to promote SKBr3 cell growth but reduce MCF-7 cell growth.

159 In contrast, MCF-7 cells had 7- and 65-day growth delays in the 50 an

160 e Cav-1 null MCF-7 cells, and PIV-5 grown in MCF-7 cells had a reduced infectivity.

161 We have previously demonstrated that MCF-7 cells, human breast cancer cells, exhibit the roll

162 ession of tissue factor cDNA was achieved in MCF-7 cells, implying that the 3'-UTR of the tissue fact

163 toxicity and enhance accumulation of ZnPc in MCF-7 cells, improving apoptotic cell death upon irradia

164 lso inhibited self-assembly of KGN, NHF, and MCF-7 cells in a dose-dependent manner that was specific

165 s on the proliferation of estrogen-dependent MCF-7 cells in a dose-dependent manner, primarily as a l

166 on of JARID1B resulted in an accumulation of MCF-7 cells in G(1).

167 S105-ERbeta levels increased in MCF-7 cells in response to 17beta-estradiol, the ERbeta-

168 ft agar and suppresses the tumorigenicity of MCF-7 cells in severe combined immunodeficiency mice.

169 pCAM/LC-SPDP/Au based biosensor could detect MCF-7 cells in the range of 1x10(5)-1x10(8) with correla

170 To investigate this, we used MCF-7 cells, in which EGF-induced transient ERK activati

171 ere screened for cytoprotective potential in MCF-7 cells, including the mitochondrial membrane potent

172 Overexpression of nuclear-targeted AKT1 in MCF-7 cells increased cell proliferation without comprom

173 The motility of MCF-7 cells increases following expression of a human PM

174 by blockade of beta-adrenergic signaling in MCF-7 cells, indicating that catecholamines were the res

175 quantification of pY in human breast cancer MCF-7 cells, indicating that pY increased by 1.60 nmol (

176 sphorylation of HER1, HER2, HER3 and HER4 in MCF-7 cells, indicative of activation of these proteins.

177 ic expression of functionally active PAR1 in MCF-7 cells induced a hormone-refractory, invasive pheno

178 , expression of BCL-2 blocks death of C6 and MCF-7 cells induced by dominant-negative ATF5, and deple

179 Here, we found that IGF-1 treatment of MCF-7 cells induced rapid ERalpha methylation by the arg

180 Furthermore, MCF-7 cells intermixed with 1 mL blood and loaded onto l

181 pic expression of EPSTI1 in the non-invasive MCF-7 cells is sufficient to induce the cell invasion.

182 Estrogen receptor-positive MCF-7 cells lack caspase-3 and were not responsive to GA

183 Human MCF-7 cells lacking functional FADS2-mediated Delta6-des

184 It subsequently interacted with the MCF-7 cell layer, distributed in the lung, heart and fat

185 CTP by short hairpin RNA in breast carcinoma MCF-7 cells leads to the declined repair efficiency for

186 ive activation of CXCR4 in poorly metastatic MCF-7 cells led to enhanced tumor growth and metastases

187 vivo biologic specificity was assessed in a MCF-7 cell line and in mice bearing MCF-7 breast tumors.

188 8 out of 10 fusion events identified in the MCF-7 cell line in an earlier study.

189 aving PTEN promoter methylated (as in, e.g., MCF-7 cell line).

190 n neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depe

191 ide population (NSP or main population) from MCF-7 cell line, and evaluated the impact of CCN5 on the

192 rmacologic properties were documented in the MCF-7 cell line, and prolactin synthesis was assessed in

193 nstrated profound cytotoxic activity against MCF-7 cell line.

194 in decreased expression of miRNA-200b in the MCF-7 cell line.

195 atively low utilization in the less invasive MCF-7 cell line.

196 A case study on data from MCF-7 cell-line reveals that PEDAL can identify successf

197 micromolar level against the HT-29, M21, and MCF-7 cell lines and blocked cell cycle progression in S

198 Conversely, stable MCF-7 cell lines expressing inducible high levels of ect

199 ork reports the impedance characteristics of MCF-7 cell lines treated with anticancer drug ZD6474 to

200 in solitary cells of GM14667, MDA-MB-231 and MCF-7 cell lines, achieving a DNA amplification efficien

201 ited the strongest cytotoxicity against both MCF-7 cell lines, over 2-fold greater than CA and Lgr, a

202 three-fold and two-folds against Caco-2 and MCF-7 cell lines, respectively.

203 oderate cytotoxic activity against HepG2 and MCF-7 cell lines.

204 owed energy production pathways to be key in MCF-7 cell lines.

205 ive phenotype on minimally invasive HeLa and MCF-7 cell lines.

206 man normal (MRC-5, MCF-10A) and tumor (A549, MCF-7) cell lines using a microfluidic system.

207 tify ~20,000 phosphopeptides from 100 mug of MCF-7 cell lysate.

208 ere achieved for the detection of ERalpha in MCF-7 cell lysate.

209 Notably, in MCF-7 cell mammospheres, which display a well-defined ac

210 expression of CREB3L1 in human breast cancer MCF-7 cells markedly enhanced the sensitivity of these c

211 had previously shown that p23-overexpressing MCF-7 cells (MCF-7+p23) exhibit increased invasion witho

212 pitulated through overexpression of T-bet in MCF-7 cells (MCF-7-T-bet).

213 ibited in Adriamycin (doxorubicin)-resistant MCF-7 cells (MCF-7/adr).

214 lar adhesion molecule (EpCAM) present on the MCF-7 cell membrane.

215 vidence demonstrating that CD24 expressed on MCF-7 cell membranes is responsible for rolling of the c

216 In MCF-7 cells Oct-1 binds the iNOS promoter, recruits RNA

217 However, the ligand that induces rolling of MCF-7 cells on E-selectin has not yet been identified, a

218 microarray profiling of the transcriptome of MCF-7 cells overexpressing miR-9 identified six novel di

219 of FOXM1 by RNAi abolished estrogen-induced MCF-7 cell proliferation and overcame acquired tamoxifen

220 thoxy substituents, through in vitro assays: MCF-7 cell proliferation and VM7Luc4E2 transactivation.

221 ounced, impacts on either ERalpha binding or MCF-7 cell proliferation.

222 Overexpression of MEK5 in MCF-7 cells promoted both hormone-dependent and hormone-

223 CXCR4 overexpression in MCF-7 cells promoted estrogen independence in vivo, wher

224 diated angiogenesis after exposure to ADP or MCF-7 cells providing a potential mechanism for how aspi

225 th of the OHT(R) cells, and its depletion in MCF-7 cells reduced sensitivity to tamoxifen in vitro an

226 45-fold for MDA-MB-231 cells and 7-fold for MCF-7 cells, relative to untargeted PCCAs.

227 e evidence that HOXB7 overexpression renders MCF-7 cells resistant to tamoxifen via cross-talk betwee

228 n distal non-tumor tissue and low-metastatic MCF-7 cells, respectively.

229 c expression of constitutively active Akt in MCF-7 cells restored cell survival in S6K2-depleted cell

230 Furthermore, the depletion of MLL1 in MCF-7 cells results in a dramatic decrease of chromatin

231 a- and glucocorticoid receptor (GR)-positive MCF-7 cells revealed that GR occupies several ERalpha-bi

232 Intravital imaging of CXCR4-expressing MCF-7 cells revealed that tumor cells migrate toward blo

233 The involvement of CD24 in MCF-7 cell rolling was confirmed by the rolling behavior

234 -IIB-GFP-, and 19% of NM-IIC1-GFP-expressing MCF-7 cells show multiple bleb formation, compared with

235 strogen receptor (ER)-positive breast cancer MCF-7 cells showed that inhibitor treatment recapitulate

236 nockdown cell lines (derived from HCT116 and MCF-7 cells) showed increased apoptosis, G(2)/M arrest a

237 7 showing lower PLD2 activity, and MTLn3 and MCF-7 cells showing an elevated activity.

238 on affects breast cancer cells, we generated MCF-7 cells stably overexpressing StARD3-green fluoresce

239 OHT(R) cells and miR-221/222-overexpressing MCF-7 cells than in control cells, which suggests modula

240 Here, we investigate MCF-7 cells that are adapted to grow in acidic condition

241 breast epithelial, MCF-10A or breast cancer, MCF-7 cells that do not harbor constitutively active STA

242 MCF-7 cells that express Y14F are resistant to paclitaxe

243 In this study, we selected MCF-7 cells that stably express forms of recombinant LOX

244 In MCF-7, cells that show the lowest level of PLD2 activity

245 nd for induction of CYP1B1 transcription (in MCF-7 cells), the recruitments of p300 and AhR, although

246 protein that overexpressed on the surface of MCF-7 cells, the aptamer conjugated MBs showed a predomi

247 In contrast, once taken up by MCF-7 cells, the iodide ligand is rapidly pumped out.

248 ellular calcium also increased the growth of MCF-7 cells through an ER-dependent mechanism.

249 Here, we show that in breast cancer MCF-7 cells, TLE3, a co-repressor of the Groucho/Grg/TLE

250 herefore hypothesized that 2 could sensitize MCF-7 cells to anti-HER2 therapies.

251 Conversely, transfection of MCF-7 cells to express ROR1 reduced expression of E-cadh

252 tudies were conducted on human breast cancer MCF-7 cells to investigate both cellular uptake and cyto

253 alyzed the transcriptional response of human MCF-7 cells to retinoic acid and TGF-beta, applied indiv

254 on changed the architecture of breast cancer MCF-7 cells to that resembling MCF-10A cells, whereas ec

255 (Br)dU-carrying duplex DNA or (Br)dU-treated MCF-7 cells to UVB light could lead to the facile format

256 In MCF-7 cells transduced with Ad-GREB1 or transfected with

257 he effects of GREB1 on cell proliferation in MCF-7 cells transduced with Ad-GREB1 were also measured

258 FGFR1-amplified/ER+ breast cancer cells and MCF-7 cells transduced with FGFR1 were resistant to fulv

259 Microarray analyses of MCF-7 cells transfected with control or SMRT small inter

260 Exposure of MCF-7 cells treated with 5 to 300 nm irradiation leads t

261 interfering RNA-induced knockdown of p53 in MCF-7 cells treated with CPEC prevented cellular senesce

262 MCF-7 cells treated with EGF, ATP, extracellular calcium

263 quencing was performed on pS118-ER and ER in MCF-7 cells treated with estrogen.

264 Using an ORF kinome screen in MCF-7 cells treated with the CDK4/6 inhibitor ribociclib

265 ulted in an increase in turnover of FOXM1 in MCF-7 cells treated with the protein synthesis inhibitor

266 Super-resolution microscopy of MCF-7 cells treated with the targeted MOF system reveals

267 iple ceramide and dihydroceramide species in MCF-7 cells treated with TNFalpha occurred by up-regulat

268 sing small interfering RNA gene knockdown in MCF-7 cells triggered fibroblastic transformation and ce

269 NANOG induction promoted drug resistance in MCF-7 cells, tumor regeneration in Du145 cells and, most

270 found to reduce in vivo estrogen stimulated MCF-7 cell tumorigenesis using a xenograft mouse model.

271 bility maintenance of Rad51 requires TCTP in MCF-7 cells under normal cell culture conditions.

272 d by the decreased rolling velocities of the MCF-7 cells upon treatment with cytochalasin D (an inhib

273 level effects of 17beta-estradiol on single MCF-7 cells using Fourier transform infrared imaging spe

274 s of gene expression across time (2-96 h) in MCF-7 cell variants that were estrogen-dependent (WS8) o

275 Senescence in MCF-7 cells was associated with a G(2)- and S-phase arre

276 The cytotoxic effect of pcm in MCF-7 cells was potentiated under H(2)O(2)-induced oxida

277 Using GRO-seq in MCF-7 cells, we defined the immediate transcriptional ef

278 CoCl2-induced EMT of human breast carcinoma MCF-7 cells, we found that TEPA, a copper chelator, inhi

279 During the cell adhesion process, MCF-7 cells were consistently softer, exhibiting up to a

280 BxPC-3 cells and MCF-7 cells were engineered to overexpress a catalytical

281 n of beta-catenin from the VE-cad complex by MCF-7 cells were lower than in MDA-MB-231 cells.

282 nts indicated that the effects of 3-OST3A in MCF-7 cells were mediated by altered interactions betwee

283 micropallet arrays in the presence of blood, MCF-7 cells were mixed into whole blood and added to sma

284 These processes were restored when MCF-7 cells were treated with beta(1)-activating antibod

285 When MCF-7 cells were treated with the analogues, those resul

286 TYR (named as MCF-7-TYR) and non-transfected MCF-7 cells were used as positive and negative controls,

287 ibroblasts (3T3-L1) and human breast cancer (MCF-7) cells were pre-treated with spice extracts and th

288 d cellular cytotoxicity of B16-F10, HeLa and MCF-7 cells when pre-incubated at lower pH, indicating T

289 e of HeLa cells expressing Cx43 or Cx46, and MCF-7 cells, which endogenously express Cx43 and Cx46.

290 Of note, MCF-7 cells with acquired resistance to an IGF-1 recepto

291 th intrinsic tamoxifen resistance as well as MCF-7 cells with acquired tamoxifen and fulvestrant resi

292 C4 and C5 inhibited tamoxifen-resistant MCF-7 cells with equal potency (IC(50) = 4-8 muM) and ef

293 ost cytotoxic compound reduced the growth of MCF-7 cells with IC(50) = 0.10 muM (cisplatin, 1.6 muM;

294 Treatment of MCF-7 cells with nicotine induced cell migration, wherea

295 We combined chromosomal interaction data in MCF-7 cells with our cohesin binding data to show that c

296 In MCF-7 cells with stable RNAi-mediated suppression of JAR

297 1R activity in mitochondrial protection, and MCF-7 cells with suppressed IGF-1R activity became highl

298 Extended treatment of MCF-7 cells with tamoxifen resulted in progressively inc

299 Furthermore, co-treatment of MCF-7 cells with the PFKFB3 inhibitor and the anti-estro

300 lpha in tamoxifen- and fulvestrant-resistant MCF-7 cells, with pharmacologic inhibition of ERRalpha s