ライフサイエンスコーパス: breast cancer cell

1 A (breast epithelial cells), and MDA-MB 231 (breast cancer cells).

2 asts, NMuMG epithelial, MDA-MB-231 and MCF-7 breast cancer cells).

3 ed apoptosis screen in a PIK3CA mutant human breast cancer cell.

4 ility and invasion in mammary epithelial and breast cancer cells.

5 .2 mammary tumor cells as well as MDA-MB-231 breast cancer cells.

6 ted regulation of invasion and metastasis in breast cancer cells.

7 s for targeted delivery of 5-fluorouracil to breast cancer cells.

8 lated with the tumorigenic activity of human breast cancer cells.

9 migration and downstream cell signalling in breast cancer cells.

10 ediates uptake and PR1 cross-presentation in breast cancer cells.

11 s a useful approach to inhibit the growth of breast cancer cells.

12 sitivity in estrogen receptor-positive MCF-7 breast cancer cells.

13 in the estrogen receptor (ER)-positive MCF7 breast cancer cells.

14 colony formation potential in ERBB2-positive breast cancer cells.

15 growth of therapy-resistant triple-negative breast cancer cells.

16 l metabolomics profile impacted by Merlin in breast cancer cells.

17 ic imaging of fluorescent beads and invasive breast cancer cells.

18 and a dormant, metastatic phenotype in ER(+) breast cancer cells.

19 attenuated migration and colony formation of breast cancer cells.

20 alter migration and morphology of metastatic breast cancer cells.

21 on of ERalpha expression in ERalpha-negative breast cancer cells.

22 /RTK signaling in ErbB2-overexpressing human breast cancer cells.

23 versing the oncogenic function of miR-221 in breast cancer cells.

24 effects of mammary fibroblasts on associated breast cancer cells.

25 promote invadopodial maturation in invasive breast cancer cells.

26 entify possible addictions across a panel of breast cancer cells.

27 nt matrix degradation in invasive MDA-MB-231 breast cancer cells.

28 on of metastatic and recurrent phenotypes by breast cancer cells.

29 lated ERalpha and ERbeta expression in MCF-7 breast cancer cells.

30 m maturation and subsequent cell invasion in breast cancer cells.

31 ate level of PAK4 protein in triple negative breast cancer cells.

32 LACTB potently inhibits the proliferation of breast cancer cells.

33 vasive potential in head and neck cancer and breast cancer cells.

34 xpression in human MDA-MB-231 and murine 4T1 breast cancer cells.

35 higher efficiency than anti-miR-221 in human breast cancer cells.

36 nign breast epithelial cells or in MYST3-low breast cancer cells.

37 s) from the ErbB, IGF-1R and Met families in breast cancer cells.

38 nation, which in turn inhibits metastasis of breast cancer cells.

39 ater effects in ovarian cancer cells than in breast cancer cells.

40 intrasinusoidal infiltration of the liver by breast cancer cells.

41 herapy-sensitive and therapy-resistant human breast cancer cells.

42 rial lipid metabolism and differentiation of breast cancer cells.

43 rested migration, invasion and metastasis of breast cancer cells.

44 on of pri-miR-96 reduced compound potency in breast cancer cells.

45 o transfected biotinylated miR-200c in mouse breast cancer cells.

46 ting in a decrease in proliferation of human breast cancer cells.

47 epletion impairs the metastatic potential of breast cancer cells.

48 unction, contributes to PARPi sensitivity in breast cancer cells.

49 by up-regulating SF3B1 and SF3B3 protein in breast cancer cells.

50 lasts increased proliferation of co-cultured breast cancer cells.

51 GF-beta is pro-metastatic for the late-stage breast cancer cells.

52 equired for autophagosome clearance in human breast cancer cells.

53 pithelial phenotype in poorly differentiated breast cancer cells.

54 ls as well as from the untreated and treated breast cancer cells.

55 /HER2 in normal mammary epithelial cells and breast cancer cells.

56 9b-1/a did not drive TAM-resistance in MCF-7 breast cancer cells.

57 trated that progesterone (P4) increases CK5+ breast cancer cells.

58 mammary epithelial cells and non-aggressive breast cancer cells.

59 Different sizes of MCF-7 breast cancer cells (8 to 15 mum) were used in this stud

60 tamoxifen-sensitive and tamoxifen-resistant breast cancer cells, a tamoxifen-resistant patient-deriv

61 Here we report that breast cancer cells activate autophagy in response to pa

62 ells, also inhibit endothelial phenotypes of breast cancer cells adopted in response to a nutrient-de

63 iDZ sensor can be internalized in live MCF-7 breast cancer cells and activated by a magnetic field to

64 ing transcription-dependent TOP2 activity in breast cancer cells and at the translocation 'hotspot',

65 PAK4 protein levels are high in breast cancer cells and breast tumors, and the gene is o

66 o MDA-MB-231 and SKBR3 (overexpressing HER2) breast cancer cells and compared with release in noncanc

67 s and distribution in cultured HER2 positive breast cancer cells and human breast tumor samples.

68 at JA stabilizes endogenous SF3B1 protein in breast cancer cells and induced dissociation of the prot

69 Here, we first demonstrated that breast cancer cells and pancreatic adenocarcinoma cells

70 y captures key aspects of iron metabolism in breast cancer cells and provides a framework upon which

71 ate, (BITC) increases p53 phosphorylation in breast cancer cells and reveal an important role of ERK

72 bits the growth of mesenchymally transformed breast cancer cells and soft tissue sarcomas of diverse

73 sts, ii) spatiotemporal interactions between breast cancer cells and stromal cells, and iii) cancer-r

74 lating the epithelial-mesenchymal balance of breast cancer cells and that WT1-expressing tumours are

75 timulation had similar inhibitory effects on breast cancer cells and this inhibition was attenuated b

76 content and PAF receptor expression in human breast cancer cells and tissue.

77 the human genome, are overexpressed in some breast cancer cells and tissues but without regard to ca

78 ES) in estrogen receptor (ER) alpha-positive breast cancer cells and tumor xenografts.

79 We found that the cystine-addicted breast cancer cells and tumors have strong activation of

80 privation signatures noted in the basal type breast cancer cells and tumors.

81 s that effectively suppress proliferation of breast cancer cells and tumors.

82 effect in different subpopulations of SKBR3 breast cancer cells, and compared the results with a dru

83 diation in both a nematode in vivo model and breast cancer cells, and could potentially be utilized a

84 ed chemotactic potential for endothelial and breast cancer cells, and elicited reduced cancer cell in

85 Wnt signaling was impaired in LGR4-deficient breast cancer cells, and LGR4 knockdown resulted in incr

86 d cells, DU-145 prostate cancer cells, MCF-7 breast cancer cells, and LU-HNSCC-25 head and neck squam

87 cell lines, druggable, enriched in stem-like breast cancer cells, and resistant to chemotherapy-induc

88 Invasive growth and apoptosis resistance of breast cancer cells are associated with metastasis and d

89 In contrast, luminal-type breast cancer cells are cystine-independent and exhibit

90 Moreover, considering that diverse breast cancer cells are differently subjected to a segre

91 g than seen with EGF, provoking responses in breast cancer cells associated with differentiation rath

92 Lentiviral silencing of CBS in human breast cancer cells attenuated GSH/GSSG, total GSH, nucl

93 1q21.3 that is enriched in subpopulations of breast cancer cells bearing characteristics of tumor-ini

94 ncer, and their suggested role in modulating breast cancer cell behaviour, very little detail is know

95 ulating PRL-induced transcription as well as breast cancer cell biology.

96 tumor growth due to loss of Ptpro within the breast cancer cells but not in surrounding tissue as con

97 y inhibited proliferation in MYST3-high, ER+ breast cancer cells, but not in benign breast epithelial

98 ollagen does not alter the total motility of breast cancer cells, but simply redirects their migratio

99 actor FVIIa enhances aggressive behaviors of breast cancer cells, but the underlying signaling mechan

100 by intracardiac or intracranial injection of breast cancer cells by 90% and 72%, respectively.

101 uction could be abrogated in triple-negative breast cancer cells by inhibition of calcium-independent

102 E2 release could be abrogated in metastatic breast cancer cells by inhibition of iPLA2.

103 G elicits the metastatic outgrowth of latent breast cancer cells by promoting the localization and tr

104 ity and abrogated the stem-like phenotype of breast cancer cells by reducing the formation of mammosp

105 By using ER-negative MDA-MB-231 breast cancer cells, clonal lines were created that expr

106 t 12h for drug-susceptible and drug tolerant breast cancer cells compared to control were 50,552+/-14

107 pression of Cdc6 and Cdt1 was upregulated in breast cancer cells compared to normal breast epithelial

108 a "low-lipid" phenotype is characteristic of breast cancer cells compared with normal breast epitheli

109 ymal transition (EMT) in cystine-independent breast cancer cells conferred the cystine-addiction phen

110 By contrast, primary cultures of invasive breast cancer cells convert glutamine to glutamate which

111 MMTV- Wnt1 tumor cells or knockdown in human breast cancer cells decreased the number of functional C

112 ting RAGE shRNA knockdown in human and mouse breast cancer cells, decreased orthotopic tumor growth,

113 n of EYA1 using short hairpin RNA (shRNA) in breast cancer cells destabilizes the Myc protein and inc

114 ine and reveal that enhancers transcribed in breast cancer cells direct critical gene regulatory netw

115 t a beneficial mechanism of E+P treatment in breast cancer cells driven by transcriptional upregulati

116 a transcription in tamoxifen (TAM)-resistant breast cancer cells, ectopic expression of miR-29b-1/a d

117 ns of the active cytoskeleton, on metastatic breast cancer cells embedded in a three-dimensional coll

118 In human breast cancer cells, EVI1 silencing reduced proliferatio

119 Accordingly, LKB1-null breast cancer cells exhibited an increased ability to fo

120 2 or after treatment with exogenous rTFPI-2, breast cancer cells exhibited reduced proliferation and

121 We also found that, in both prostate and breast cancer cells, exposure to Tg or Tg analogs for 1

122 Brca1185stop tumors and human BRCA1185delAG breast cancer cells expressed a really interesting new g

123 We found that 4T1 breast cancer cells expressed high levels of CXCR7, but

124 In vitro, P4-treated breast cancer cells formed larger mammospheres and silen

125 A (shRNA)-mediated knockdown of p62 impaired breast cancer cells from self-renewing under anchorage-i

126 tice-light sheet imaging of MDA-MB-231 human breast cancer cells genetically engineered to brightly e

127 MSI2 influenced breast cancer cell growth by altering ESR1 function.

128 of the Warburg effect and the inhibition of breast cancer cell growth, which may serve as a useful a

129 nation for exercise-dependent suppression of breast cancer cell growth.

130 Here, we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-

131 with this observation, loss-of-LKB1 rendered breast cancer cells highly migratory and invasive, attai

132 In MCF-7 and ZR75.1 breast cancer cells, IGF-1 induces peroxisome proliferat

133 t enzyme of the serine synthesis pathway, in breast cancer cells impairs tumor initiation, metastasis

134 er, inhibiting BORG expression in metastatic breast cancer cells impedes their metastatic colonizatio

135 er injection of metastatic or non-metastatic breast cancer cells in 4T1.2 BALB/cJ and MDA-MB-231 nude

136 g significantly decreasing cell viability of breast cancer cells in a CL dose-dependent manner in vit

137 ta3 (beta3), which is selectively induced on breast cancer cells in bone by the local bone microenvir

138 with DAC to reduce the viability of luminal breast cancer cells in in vitro assays.

139 visualize nanotubes in situ, interconnecting breast cancer cells in live acute brain slices from an e

140 ration and activated apoptosis in MDA-MB-231 breast cancer cells in vitro and in vivo.

141 These compounds also block the growth of the breast cancer cells in vitro, and stimulate apoptosis.

142 re more effective at killing triple negative breast cancer cells in vitro.

143 of p62 enhanced the self-renewal ability of breast cancer cells in vitro.

144 uences the tumour reconstitution dynamics of breast cancer cells in vivo.

145 RFP14 treatment augments these phenotypes in breast cancer cells in which RAB25 is tumor suppressive.

146 ext generation sequencing of triple negative breast cancer cells in which the isoforms were specifica

147 ngeneic studies with orthotopically injected breast cancer cells in wild-type and RAGE-knockout C57BL

148 ey are highly cytocidal toward several human breast cancer cells, including hormone-independent and c

149 Accordingly, E+P treatment of breast cancer cells increased ER binding to the NEMO pro

150 RAGE ectopic overexpression in breast cancer cells increased MEK-EMT (MEK-epithelial-to

151 Using human exercise-conditioned serum for breast cancer cell incubation studies and murine exercis

152 nchorage-independent growth of mutant PIK3CA breast cancer cells independently of its effects on COX-

153 of IDP-ASE to human embryonic stem cells and breast cancer cells indicate that the imbalance of ASE a

154 Depleting or increasing miR-221 level in breast cancer cells induced or decreased E-cadherin prot

155 ific demethylase KDM3A played a dual role in breast cancer cell invasion and apoptosis by demethylati

156 e of the mechanisms by which TFPI-2 inhibits breast cancer cell invasion could be via the regulation

157 It has been shown that Akt activation in breast cancer cells is modulated by calmodulin (CaM).

158 nockdown with multiple independent shRNAs in breast cancer cells led to decreased transwell invasion

159 Here we report that, in breast cancer cells, liganded GR represses a large ERalp

160 , although at a higher IC50 as compared with breast cancer cells, likely due to more active ATRA meta

161 For in vivo studies, a human breast cancer cell line (MDA-231) was implanted in five

162 RB inactivation in an RB-intact luminal-type breast cancer cell line MCF-7 promoted a positive feed f

163 of field based 3D-QSAR model based on human breast cancer cell line MCF7 in vitro anticancer activit

164 To do this, we used the breast cancer cell line MCF7, which expresses a function

165 cancer cell line MDA-MB-231 and the luminal breast cancer cell line MCF7: a) a 3D collagen embedded

166 o models employing the triple-negative basal breast cancer cell line MDA-MB-231 and the luminal breas

167 ole in the migration and invasiveness of the breast cancer cell line MDA-MB-231.

168 nous leukemia cell line as well as the MCF-7 breast cancer cell line with chromatin interactions.

169 ry subunit of HIF-1 (HIF-1alpha) in a murine breast cancer cell line, EMT6.

170 le as well as detection from real samples of breast cancer cell line, MCF-7.

171 f 485 single nuclei to 424 single cells in a breast cancer cell line, which shows a high concordance

172 rom the NA12878 human genome and the HCC1954 breast cancer cell line.

173 yrosine 537, in the estrogen-responsive MCF7 breast cancer cell line.

174 ty during a time course of a hypoxia-exposed breast cancer cell line.

175 l as differences in the mechanotype of human breast cancer cell lines (Ea = 2.1 +/- 0.1 and 0.80 +/-

176 us to discriminate between normal and human breast cancer cell lines (fibrocystic and metastatic sta

177 fold more potent at inhibiting the growth of breast cancer cell lines (MCF7, MCF7/VP16, BT474, T47D,

178 e initial cell line panel to now include the breast cancer cell lines (MCF7, MCF7/VP16, BT474, T47D,

179 ysis in i) normal colon cells, ii) colon and breast cancer cell lines and iii) cancer stem-like cell

180 3 signals constitutively in a panel of basal breast cancer cell lines and in more than one third of b

181 me analysis' (IMAHP) method to a panel of 41 breast cancer cell lines and show that deviations of the

182 proteins were positively correlated in human breast cancer cell lines and tissue specimens of primary

183 lator Id4 This signature drove clustering of breast cancer cell lines and tumors into the common subt

184 rbon monoxide (CO) reduced GSH/GSSG in three breast cancer cell lines by inhibiting CBS.

185 addition, some of RB-intact basal-like type breast cancer cell lines exhibited a similar phenotype f

186 To investigate this question, we developed breast cancer cell lines expressing an inducible, consti

187 We selected lung and breast cancer cell lines for the ability to infiltrate a

188 R/Cas9 has no effect on the fitness of basal breast cancer cell lines or cell lines from six other ca

189 a-nuclear accumulation of the PRMT5/WDR77 in breast cancer cell lines relative to immortalized breast

190 nomes (using ChIP-seq) of 11 different human breast cancer cell lines representing five major molecul

191 A validation study on 21 breast cancer cell lines showed that our prediction agre

192 18)F-FASu demonstrated tumor uptake in all 3 breast cancer cell lines studied.

193 on 11 of 19 ovarian cancer (OC) and 8 of 14 breast cancer cell lines tested.

194 defects by direct and indirect assays in 12 breast cancer cell lines to estimate the spontaneous occ

195 e investigated the sensitivity of a panel of breast cancer cell lines to treatment with various types

196 A panel of breast cancer cell lines was treated with increasing con

197 eatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion an

198 h GSK1016790A reduced viability of two basal breast cancer cell lines with pronounced endogenous over

199 ical CTC phenotype more lysis-resistant than breast cancer cell lines, a capacity to report protein e

200 NAs, miR-221 and miR-17, are tested in human breast cancer cell lines, demonstrating the 70 approxima

201 1 in total RNA extracted from human lung and breast cancer cell lines, discriminating between the can

202 nation therapy because they are essential in breast cancer cell lines, druggable, enriched in stem-li

203 In breast cancer cell lines, increased levels of centrosome

204 an extensive gene expression analysis in ER+ breast cancer cell lines, to reveal the targets of miR-5

205 lidated our findings in MCF-7 and MDA-MB-231 breast cancer cell lines, which harbor lower hsa-miR-125

206 cells (HMECs) and estrogen receptor-positive breast cancer cell lines.

207 R1 deficit in colorectal, ovarian, renal and breast cancer cell lines.

208 oach to globally profile CARM1 substrates in breast cancer cell lines.

209 tent stem cells with conditioned medium from breast cancer cell lines.

210 nd seven of these exhibited synergy in human breast cancer cell lines.

211 ncreased apoptosis in a panel of ER-positive breast cancer cell lines.

212 liparib and radiation on metabolism in three breast cancer cell lines.

213 icantly altered metformin sensitivity in two breast cancer cell lines.

214 hairpin RNA (shRNA) "dropout screens" on 77 breast cancer cell lines.

215 and multiple additional estrogen-independent breast cancer cell lines.

216 d greater growth-inhibitory activity against breast cancer cell lines.

217 tic cancer tissues as well as pancreatic and breast cancer cell lines.

218 ll cycle arrest, and cell death in sensitive breast cancer cell lines.

219 we demonstrate that targeting of p38delta in breast cancer cells, MCF-7 and MDA-MB-231 resulted in a

220 270), human embryonic kidney cells (HEK) and breast cancer cells (MCF7) we showed that Verteporfin-in

221 elial-mesenchymal transition and stemness in breast cancer cells-mechanisms critical to tumorigenesis

222 mice transplanted tumor model indicated that breast cancer cells Met-1 with up-regulation of DACH1 we

223 Endothelial cells promote triple-negative breast cancer cell metastasis via PAI-1 and CCL5 signali

224 of Chrdl1 to block BMP-induced increases in breast cancer cell migration and invasion.

225 so report that PHF8 plays important roles in breast cancer cell migration and tumor growth.

226 o in endothelial, lymphatic endothelial, and breast cancer cell migration assays.

227 crosis, but not apoptosis, in the basal-type breast cancer cells mostly seen in TNBC tumors.

228 rom WAT progenitors, and GM-CSF knockdown in breast cancer cells neutralized the protumorigenic activ

229 Breast cancer cells often develop resistance to endocrin

230 a, and triggers apoptosis of triple negative breast cancer cells only under hypoxic conditions.

231 l transcriptional target of E+P signaling in breast cancer cells, our work offers a mechanistic expla

232 The breast cancer stem cell (CSC) and bulk breast cancer cell potency of a series of metallopeptide

233 values can be correlated with the number of breast cancer cells present in the sample, we suggest th

234 In our experiments, human breast cancer cells primarily assimilated ammonia throug

235 tin inhibition of MDA-MB-231 triple-negative breast cancer cell proliferation and tumor growth.

236 study, we showed that loss of DLG5 promoted breast cancer cell proliferation by inhibiting the Hippo

237 gest that miR-29 repression of TAM-resistant breast cancer cell proliferation is mediated in part thr

238 h the IL4Ralpha antagonist IL4DM compromised breast cancer cell proliferation, invasion, and tumor gr

239 nstrate that overexpression of VGLL4 reduces breast cancer cell proliferation, migration, intravasati

240 Parkin downregulation in breast cancer cells promotes metastasis, which can be in

241 We find that malignant breast cancer cells readily transfer to new collagen I s

242 NgBR knockdown in human breast cancer cells reduces Ras membrane localization, i

243 pithelial to mesenchymal transition (EMT) in breast cancer cells regulates metastasis, stem cell prop

244 rom distinct basolateral membrane domains in breast cancer cells, resulting in a less transformed phe

245 ion and inhibits the self-renewal ability of breast cancer cells, resulting in an attenuated CD44(+)/

246 show that triggering of stromal NOTCH-MYC by breast cancer cells results in a POL3-driven increase in

247 Ribociclib-resistant breast cancer cells selected by chronic drug exposure di

248 ne network" that couples specific aspects of breast cancer cell shape to signaling and transcriptiona

249 wer level than Akt3/+S472 in triple-negative breast cancer cells, specific ablation of Akt3/-S472 enh

250 face, the cyclic peptide was able to capture breast cancer cells specifically and sense samples with

251 RNA and increased with p62 overexpression in breast cancer cells, suggesting that p62 positively regu

252 eostasis and is critical for triple-negative breast cancer cell survival.

253 estigate the unique transhesive profiles for breast cancer cells that are adapted to colonize differe

254 However, aggressive breast cancer cells that manifest TET2-miR-200c dysregul

255 Here, we characterize, in breast cancer cells, the molecular effects of a recently

256 Indeed, when CXCR7 was silenced in breast cancer cells, their metastatic ability was inhibi

257 etabolism and the differentiation program of breast cancer cells, thereby revealing a previously unde

258 trations, suppresses invasiveness of luminal breast cancer cells through the estrogen receptor (ER).

259 Targeting IL4 signaling sensitized breast cancer cells to anticancer therapy and strengthen

260 n-2/TGFbeta/CSF-1 signaling axis employed by breast cancer cells to capture host macrophage functions

261 rexpression of miR-15a and miR-16 sensitized breast cancer cells to DNA damage induced by the chemoth

262 A repair while elevated levels can sensitize breast cancer cells to doxorubicin leading to apoptotic

263 Furthermore, CO sensitized breast cancer cells to doxorubicin.

264 de that non-canonical DDR1 signaling enables breast cancer cells to exploit the ubiquitous interstiti

265 found that miR-152 expression sensitized the breast cancer cells to paclitaxel treatment by inhibitin

266 ant increase in CPEB2B was also required for breast cancer cells to resist cell death because of deta

267 ow that serum withdrawal induces mesenchymal breast cancer cells to undergo VM and that knockdown of

268 trogen receptor-positive and triple-negative breast cancer cell types.

269 Upon transfer to breast cancer cells, unshielded RN7SL1 activates the PRR

270 mpact of autophagy on the pathophysiology of breast cancer cells using a novel hypoxia-dependent, rev

271 ures in the electrochemical readout of MCF-7 breast cancer cells versus MCF-10A mammary epithelial ce

272 A, by fragmenting mouse bones preloaded with breast cancer cells via intra-iliac artery injection.

273 sitive) and MDA-MB-231 (hormone-insensitive) breast cancer cell viability in vitro by 11% to 19% and

274 d norepinephrine (NE) could directly inhibit breast cancer cell viability, as well as tumor growth in

275 Overall, our results show how IL30 regulates breast cancer cell viability, migration, and gene expres

276 tes in lysates of 100, 1000, and 10000 MCF-7 breast cancer cells was carried out using a new labeling

277 The deformability of MCF-7 breast cancer cells was characterized based on the passa

278 2 8.02 d), and their activity in MCF-7 human breast cancer cells was studied.

279 S nanoparticles that target HER2 and CD44 in breast cancer cells, we demonstrate labeling of fixed ce

280 Using chemical probes and MDA-MB-231 breast cancer cells, we found here that the inhibitors o

281 is of the ER cistrome in tamoxifen-resistant breast cancer cells, we have uncovered a role for an RUN

282 imental tumor construct, MCF7 and MDA-MB-231 breast cancer cells were coinjected into the mammary fat

283 Breast cancer cells were incubated with DOX azide and (6

284 tumorigenesis by 50% when preincubated MCF-7 breast cancer cells were inoculated into NMRI-Foxn1(nu)

285 coma cells and MT1-MMP function in MDA-MB231 breast cancer cells were not affected by DDR kinase inhi

286 Motile breast cancer cells were pre-seeded into the collagen ma

287 es with cortactin to invadopodia of invasive breast cancer cells, where it mediates epidermal growth

288 as engineered to specifically bind and enter breast cancer cells, where successful tumor targeting wa

289 e, we have identified a mechanism, unique to breast cancer cells, whereby cystathionine beta-synthase

290 ammary fat pad after transfecting MDA-MB-231 breast cancer cells, while BMD cells were isolated from

291 Treatment of breast cancer cells with a miR-139-5p mimic strongly syn

292 DD) remarkably inhibited the growth of human breast cancer cells with little toxicity.

293 we demonstrate that treatment of human MCF-7 breast cancer cells with pro-inflammatory cytokines resu

294 Breast cancer cells with stem cell properties are key co

295 d-amino acid (k) displayed higher uptake by breast cancer cells, with minimal uptake by the noncance

296 analyzed the intravasation of invasive human breast cancer cells within a tissue-engineered microvess

297 to enhance delivery of chemotherapeutics to breast cancer cells within the bone by exploiting their

298 e rapidly in a xenograft model of irradiated breast cancer cells; Wwox-deficient cells exhibited sign

299 In some breast cancer cells, xCT antiporter expression is upregu

300 or pituitary, or the proliferation of MCF-7a breast cancer cell xenografts.