ライフサイエンスコーパス: prostate cancer cell

1 and causes growth retardation in a panel of prostate cancer cells.

2 larifies the molecular radiation response of prostate cancer cells.

3 kinase proteins in a pair of bone metastatic prostate cancer cells.

4 resistance to genotoxic stress in aggressive prostate cancer cells.

5 ize and epigenetic states between normal and prostate cancer cells.

6 geting KPNB1 suppressed the proliferation of prostate cancer cells.

7 PAICS is required for growth and survival of prostate cancer cells.

8 ating NF-kappaB in a Rho-dependent manner in prostate cancer cells.

9 olic adaptation and castration-resistance of prostate cancer cells.

10 essed between Caucasian and African American prostate cancer cells.

11 EAF2 in androgen regulation of DNA repair in prostate cancer cells.

12 en protection of DNA damage via Ku70/Ku80 in prostate cancer cells.

13 f multiple AR-positive, but not AR-negative, prostate cancer cells.

14 ERK pathway to promote NE differentiation of prostate cancer cells.

15 transduction-induced phenotypic switching of prostate cancer cells.

16 sion, proliferation, and malignant growth of prostate cancer cells.

17 sion of MDSC-promoting cytokines secreted by prostate cancer cells.

18 utes causatively to the invasive motility of prostate cancer cells.

19 or primary and secondary sphere formation of prostate cancer cells.

20 -1beta and IL-18 were confined to aggressive prostate cancer cells.

21 tively controls mitochondrial respiration in prostate cancer cells.

22 arget genes in the androgen-responsive LNCaP prostate cancer cells.

23 loop in both CRPC and enzalutamide-resistant prostate cancer cells.

24 anscription of the androgen receptor (AR) in prostate cancer cells.

25 in regulating the migration and invasion of prostate cancer cells.

26 itigate oncogenic function of SUB1 in benign prostate cancer cells.

27 abinoid receptor 2 (CB2) in human breast and prostate cancer cells.

28 23b/-27b-mediated repression of migration in prostate cancer cells.

29 nd hindered tumorigenicity of radioresistant prostate cancer cells.

30 and type I IFN production in mouse and human prostate cancer cells.

31 nd inhibits skeletal metastasis formation of prostate cancer cells.

32 in reactivation of transposable elements in prostate cancer cells.

33 rial nucleoside diphosphate kinase (NDPK) in prostate cancer cells.

34 egulate hormone-dependent gene expression in prostate cancer cells.

35 ived EVs and studied their interactions with prostate cancer cells.

36 prostate, as well as growth and survival of prostate cancer cells.

37 minate them from exosomes derived from LNCaP prostate cancer cells.

38 Here, we investigate the role of PHF19 in prostate cancer cells.

39 tability and changing DNA repair capacity in prostate cancer cells.

40 LIFR) signaling induced SUCLG2 expression in prostate cancer cells.

41 d survival, migration, and invasion in human prostate cancer cells.

42 signaling in regulating the transcriptome of prostate cancer cells.

43 ctive effects on the miRNome and proteome in prostate cancer cells.

44 riant of SELEX, on exosomes secreted by VCaP prostate cancer cells.

45 invasive potential of enzalutamide-resistant prostate cancer cells.

46 teractions in normal prostate epithelial and prostate cancer cells.

47 ubsequent decrease in proliferation of human prostate cancer cells.

48 e epithelial-mesenchymal transition (EMT) in prostate cancer cells.

49 in mouse prostatic epithelium to mimic human prostate cancer cells.

50 alpha) controls the aggressive properties of prostate cancer cells.

51 ctivation of AKT attenuated glycolysis in AA prostate cancer cells.

52 or PGC1 drives invasiveness and migration of prostate cancer cells.

53 Murine-reconstituted, oncogene-driven prostate cancer cells (0.1 x 10(6)) (RM1), transduced to

54 ecretion of exosomes that enable invasion of prostate cancer cells across extracellular matrix barrie

55 find depletion of FASN expression increases prostate cancer cell adhesiveness, impairs HGF-mediated

56 miR-214 expression in prostate cancer cells also inhibited cell migration and

57 nd separate either one red blood cell or one prostate cancer cell and facilitate the simultaneous mea

58 A2 SAM domain (EphA2DeltaS) in DU145 and PC3 prostate cancer cells and a skin tumor cell line derived

59 al modulator for altered MMP-3 expression in prostate cancer cells and CAFs, but through different re

60 r several orders of magnitude between single prostate cancer cells and how PSA expression shifts with

61 ty in vitro and in human glioma, breast, and prostate cancer cells and in v-Src-transformed murine fi

62 es c-Myc signaling in enzalutamide-resistant prostate cancer cells and inhibition of 5-Lox by Quiflap

63 regulates the tumorigenicity of AR-positive prostate cancer cells and is a promising therapeutic tar

64 d by stromal cells activates invasiveness of prostate cancer cells and may play a role in driving tum

65 as a cognate inhibitor for TMPRSS2 in human prostate cancer cells and may serve as a potential facto

66 so explored the effects of nicotine in human prostate cancer cells and prostate cancer-prone TRAMP mi

67 -sensitized naive and enzalutamide-resistant prostate cancer cells and reduced AR and AR-V7 levels to

68 d genome editing reduces HDL uptake into the prostate cancer cells and reduces their proliferation in

69 rate how RAGE-PR3 interactions between human prostate cancer cells and the bone marrow microenvironme

70 n CSLPHNPs) re-sensitizes castrate resistant prostate cancer cells and tumors to docetaxel, allowing

71 RP activity is essential for the survival of prostate cancer cells and we demonstrate a synthetic let

72 Vitamin K inhibits prostate cancer cells, and an altered expression of vita

73 fferent phenotypes in a population of murine prostate cancer cells, and describes the hysteresis in t

74 Here, we found that JMJD1A knockdown in prostate cancer cells antagonizes their proliferation an

75 nt expression of CHPT1 gene in Enz-sensitive prostate cancer cells, AR binds to a different enhancer

76 in regulating proliferation and survival of prostate cancer cells by controlling c-Myc expression at

77 nism by which AR alters the transcriptome of prostate cancer cells by modulating alternative splicing

78 pondin 2 (an MMP-3 suppressor) expression in prostate cancer cells by upregulating microRNA-128.

79 environment exerts a pro-invasive effect on prostate cancer cells, by activating a previously unexpl

80 d for controlling of IL-1beta expression and prostate cancer cell colony growth in soft agar.

81 s in the stromal tumor microenvironment in a prostate cancer cell-conditioned media model.

82 The lack of p-Drp1(S616) in AA prostate cancer cells contributed to defective cytochrom

83 or the first time, that TSPAN1 expression in prostate cancer cells controls the expression of key pro

84 1 inhibitor (116-9e) in castration-resistant prostate cancer cell (CRPC) and spheroid models.

85 In both three-dimensional primary prostate cancer cell cultures that are prone to Gravin d

86 lls and controls, miR-23b/-27b expression in prostate cancer cells decreased seminal vesicle invasion

87 In AA prostate cancer cells, decreased nuclear accumulation of

88 ctivity, while in vitro experiments in three prostate cancer cells demonstrated that this pair of com

89 mediated gene editing of CXCR7 revealed that prostate cancer cells depend on CXCR7 for proliferation,

90 clusion, downregulation of PGC1alpha renders prostate cancer cells dependent on polyamine to promote

91 Furthermore, blocking endogenous TBX2 in prostate cancer cells dramatically reduced bone-colonizi

92 antitumor activity against hormone-resistant prostate cancer cells (DU145) relative to triptorelin.

93 Prostate cancer cells (DU145) spiked into a sample with

94 an skin fibroblast cells (AGO1522) and human prostate cancer cells (DU145).

95 pression of MMP-3 in stromal fibroblasts and prostate cancer cells during tumor progression, clarifyi

96 sistently, PLK1 downregulation in metastatic prostate cancer cells enhances epithelial characteristic

97 It is well known that the bulk of prostate cancer cells express androgen receptor (AR) and

98 he diversity of tumor-initiating cells, most prostate cancer cells express the androgen receptor (AR)

99 Prostate cancer cells expressing alpha6 integrin (DU145

100 ta suggests that nutrient deprivation primes prostate cancer cells for adaptability to oxidative stre

101 Furthermore, SR-B1(-/-) prostate cancer cells formed smaller tumors in WT hosts

102 Androgens are known to protect prostate cancer cells from DNA damage.

103 h, and ERF loss rescues TMPRSS2-ERG-positive prostate cancer cells from ERG dependency.

104 t adiponectin does not protect colorectal or prostate cancer cells from radiation-induced death.

105 The gene expression profile of human prostate cancer cells from The Cancer Genome Atlas revea

106 Canonically, MYC up-regulation in luminal prostate cancer cells functions to oppose the terminally

107 origenic effect of KLF4 extends to PC3 human prostate cancer cells growing in the bone.

108 Knock-down of plectin inhibits prostate cancer cell growth and colony formation in vitr

109 te that plectin is an important regulator of prostate cancer cell growth and metastasis.

110 e a role of HGF/MET in beta-catenin-mediated prostate cancer cell growth and progression and implicat

111 BET bromodomain inhibitors block prostate cancer cell growth at least in part through c-M

112 ere, we provide evidence that PRMT5 promotes prostate cancer cell growth by epigenetically activating

113 ate the paradoxical role that GPC-1 plays in prostate cancer cell growth by interacting with stromal

114 in JMJD1A-knockdown cells partially rescued prostate cancer cell growth in vitro and in vivo.

115 prostate cancer and that miR-32 can improve prostate cancer cell growth in vitro.

116 significantly decreases FOXA1 expression and prostate cancer cell growth.

117 Breast and prostate cancer cells home to the bone marrow, where the

118 Silencing of IDH2 in prostate cancer cells impaired oxidative bioenergetics,

119 , we performed a cell tracking experiment of prostate cancer cells in a PLA device for advanced cell

120 However, prostate cancer cells in advanced stages become resistan

121 lity of luciferase reporter systems in C4-2B prostate cancer cells in mono-culture and in co-culture

122 ert differential effects on proliferation in prostate cancer cells in response to TGF-beta, and inhib

123 ys a key role in maintaining the dormancy of prostate cancer cells in the bone microenvironment.

124 to decrease proliferation and metastasis of prostate cancer cells in vitro and in vivo murine xenogr

125 rved that macrophage-driven efferocytosis of prostate cancer cells in vitro induced the expression of

126 PR3 bound to RAGE on the surface of prostate cancer cells in vitro, inducing tumor cell moti

127 B1 WT (SR-B1(+/+)) and SR-B1 KO (SR-B1(-/-)) prostate cancer cells in WT and apolipoprotein-AI KO (ap

128 ensitivity) and will not be expressed on non-prostate-cancer cells in the sample (giving high specifi

129 ltered the splicing of at least 557 genes in prostate cancer cells, including AR.

130 Knockdown of MYC expression in prostate cancer cells increased the expression of MEIS1

131 th inhibitory effects of JMJD2A depletion in prostate cancer cells, indicating that YAP1 is a downstr

132 Importantly, miR-214 overexpression in prostate cancer cells induced apoptosis, inhibiting cell

133 Coculture experiments revealed that prostate cancer cells induced the expression of inhibito

134 We assessed the consequences of prostate cancer cell interaction with neural cells, whic

135 figurations were tested by spiking breast or prostate cancer cells into murine blood, and both detect

136 filaments by the drebrin/EB3 pathway drives prostate cancer cell invasion and is therefore implicate

137 n response to guidance cues, plays a role in prostate cancer cell invasion.

138 vation, extracellular matrix degradation and prostate cancer cell invasion.

139 Increased HIP1R expression in prostate cancer cells inversely phenocopied the effects

140 corroborates that the lineage status of the prostate cancer cells is a determinant for its propensit

141 hat the upregulation of MAP4K4 in metastatic prostate cancer cells is driven by the MYC proto-oncogen

142 34a and chemosensitizes paclitaxel-resistant prostate cancer cells, killing both cancer stem-like cel

143 Depletion of PKIA in prostate cancer cells leads to reduced migration, increa

144 e inhibition of HK2-mitochondrial binding in prostate cancer cells led to decreased viability.

145 derived from a primary tumour-derived human prostate cancer cell line (OPCT-1), and its use to explo

146 y estimates cell cycle peak times in a human prostate cancer cell line and it correctly identifies tw

147 We applied ScanNeo in a prostate cancer cell line and validated our predictions

148 We found PTEN depletion in the prostate cancer cell line DU145 did not detectably impac

149 ork, we studied gene transfection of a human prostate cancer cell line exposed to megahertz pulsed ul

150 on experiments confirmed that CENPA promotes prostate cancer cell line growth.

151 prostate cancer and genome-wide studies in a prostate cancer cell line indicate that ETV4 and MED25 o

152 Introduction of PTEN into a PTEN null prostate cancer cell line leads to dephosphorylation of

153 primary MSCs with validated bone metastatic prostate cancer cell line models.

154 redicted regulatory SNPs and target genes in prostate cancer cell line models.

155 Studies of the STAT3-deficient prostate cancer cell line PC-3 (PC3) along with STAT3-pr

156 ient to enhance the metastatic phenotypes of prostate cancer cell line PC-3 in vivo.

157 metabolic differences between the aggressive prostate cancer cell line PC3 and the even more aggressi

158 ic myeloid leukaemia cell line; and DU145, a prostate cancer cell line): silencing SP1 decreased AGAP

159 In the current study, we use a human prostate cancer cell line, LNCaP as a model to perform w

160 cific target as well as proliferation in the prostate cancer cell line, LNCaP.

161 ive activity in the androgen-independent PC3 prostate cancer cell line.

162 ges in histone lysine methylation in a human prostate cancer cell line.

163 duces the opposite result in a more indolent prostate cancer cell line.

164 somes derived from healthy human serum and a prostate cancer cell line.

165 vivo models of the GRPR-positive, PC-3 human prostate cancer cell line.

166 performed with mice bearing LNCaP and PC-3 (prostate cancer cell line; PSMA-negative) tumors.

167 tested SiNVICT on simulated data as well as prostate cancer cell lines and cfDNA obtained from castr

168 Drebrin is also upregulated in human prostate cancer cell lines and co-localizes with actin f

169 ducing the AR protein level by >95% in these prostate cancer cell lines and effectively suppressing A

170 were increased in both castration-resistant prostate cancer cell lines and in primary tumors.

171 ly inhibits cell growth in these AR-positive prostate cancer cell lines and is >100 times more potent

172 As a result, prostate cancer cell lines and organoids derived from in

173 dation and accumulation of these proteins in prostate cancer cell lines and patient specimens and cau

174 were investigated using quantitative PCR for prostate cancer cell lines and primary tumors.

175 fold heterogeneity in AR output within human prostate cancer cell lines and show that cells with high

176 , has been reported to upregulate the UPR in prostate cancer cell lines and to slow their growth.

177 quence, 5-AzadC induced HEXIM1 expression in prostate cancer cell lines and triple negative breast ca

178 ro antitumor activity toward three different prostate cancer cell lines and was able to induce 60% tu

179 7A1, reduced cellular cholesterol content in prostate cancer cell lines by inhibiting the activation

180 In vitro studies in human prostate cancer cell lines demonstrated that transient o

181 Prostate cancer cell lines derived from HiMyc tumors (HM

182 the effects of HSP90 inhibition on AR-V7 in prostate cancer cell lines endogenously expressing this

183 We also found that metastatic prostate cancer cell lines have a reduced level of Ate1

184 knockdown increases or decreases invasion of prostate cancer cell lines in 3D in vitro assays, respec

185 to actin filaments, reduced the invasion of prostate cancer cell lines in 3D in vitro assays.

186 nding to drebrin, also inhibited invasion of prostate cancer cell lines in 3D in vitro assays.

187 ces degradation of AR protein in AR-positive prostate cancer cell lines in a dose- and time-dependent

188 D9 subunit, is required for the viability of prostate cancer cell lines in vitro and for optimal xeno

189 activity suppressed the invasive capacity of prostate cancer cell lines in vitro and in vivo Mechanis

190 the proliferation of multiple AR-expressing prostate cancer cell lines including those that failed t

191 potent inhibitory effects on both PACE4 and prostate cancer cell lines proliferation.

192 Further investigation in three different prostate cancer cell lines singled out pro-tumorigenic C

193 high expression of GPC-1 in more aggressive prostate cancer cell lines such as PC-3 and DU-145.

194 Prostate cancer cell lines that induce mixed osteoblasti

195 ockout (KO) of SR-B1 in both human and mouse prostate cancer cell lines through CRISPR/Cas9-mediated

196 Genetic modulation of PPARD in human prostate cancer cell lines validated the tumor suppressi

197 and extracellular metabolic profiles of four prostate cancer cell lines with varying degrees of aggre

198 traversed the plasma membrane of breast and prostate cancer cell lines, and elicited reporter-gene e

199 d epithelial-mesenchymal transition in human prostate cancer cell lines, and stable overexpression of

200 ice performance was characterized using four prostate cancer cell lines, including PC-3, VCaP, DU-145

201 6, and 10.4 nM in LNCaP, VCaP, and 22Rv1 AR+ prostate cancer cell lines, respectively.

202 Using a panel of prostate cancer cell lines, we demonstrated that MYC sup

203 Using prostate cancer cell lines, we showed that INPP4B regula

204 Using a series of experiments in human prostate cancer cell lines, we validate the highest rank

205 ased CXCR7 expression in androgen-responsive prostate cancer cell lines, which was accompanied by enh

206 decreased migration and invasion of various prostate cancer cell lines.

207 onal start site of LTF is hypermethylated in prostate cancer cell lines.

208 terization and drug testing in a panel of 20 prostate cancer cell lines.

209 and verified their mRNA level in a panel of prostate cancer cell lines.

210 l of cancer cell lines, particularly against prostate cancer cell lines.

211 ir cytotoxicity against ovarian, breast, and prostate cancer cell lines.

212 androgen-insensitive and androgen-responsive prostate cancer cell lines.

213 nuclear entry and functions in several human prostate cancer cell lines.

214 .g. MYC and POU5F1B) were identified in both prostate cancer cell lines.

215 ately active against aggressive melanoma and prostate cancer cell lines.

216 ultrasound-induced cytotoxicity against both prostate cancer cell lines.

217 ient samples by the TCGA are mirrored in the prostate cancer cell lines.

218 ity in independently derived LNCaP and LAPC4 prostate cancer cell lines.

219 naling and neuroendocrine differentiation of prostate cancer cell lines.

220 a genome-wide CRISPR-Cas9 screen using LNCaP prostate cancer cells, loss of co-repressor TLE3 conferr

221 Knockdown of 12-HETER1 in prostate cancer cells markedly reduced colony formation

222 s red blood cells, white blood cells, DU-145 prostate cancer cells, MCF-7 breast cancer cells, and LU

223 -dependent repression of ERRgamma reprograms prostate cancer cell metabolism to favor mitochondrial a

224 Expression of miR-23b/-27b decreases prostate cancer cell migration, invasion and results in

225 the data show that myosin IC is involved in prostate cancer cell migration, migration outside extrac

226 CRISPR/Cas9 knockout revealed that, in human prostate cancer cells, miR-1205 promoted cell proliferat

227 d two anti-androgen and castration resistant prostate cancer cell models that do not rely on AR activ

228 endogenous TBX2 expression in PC3 and ARCaPM prostate cancer cell models using a dominant-negative co

229 CARBs can serve as a prostate cancer cell-of-origin upon Pten deletion, yield

230 to bone, whereas HER2 supports the growth of prostate cancer cells once they are established at metas

231 Indeed, Rac1-null PC3 prostate cancer cells or cancer models with low levels o

232 s 3T3-L1 with androgen-sensitive LNCaP human prostate cancer cells, or by culturing LNCaP cells in ad

233 Here, we demonstrated that in resistant prostate cancer cells overexpressing EGFR, it was capabl

234 lates the migration and invasion of cultured prostate cancer cells, partially by modulating the activ

235 lium-labeled HZ220 was characterized in PC-3 prostate cancer cells (PC-3), and tumor uptake in mice w

236 n vitro, we found honey is cytotoxic towards prostate cancer cells PC3 and DU145.

237 Furthermore, c-Myc knockdown in prostate cancer cells phenocopied effects of JMJD1A knoc

238 strating the impact of mechanical signals on prostate cancer cell phenotypes.

239 ne-independent survival and proliferation of prostate cancer cells post androgen ablation.

240 r tumors reduces HDL-associated increases in prostate cancer cell proliferation and disease progressi

241 PCAT1 promotes prostate cancer cell proliferation and tumor growth in v

242 Mechanistically, miR-214 inhibited prostate cancer cell proliferation by targeting protein

243 -3(2H)-one (5b) that inhibited in vitro PC-3 prostate cancer cell proliferation with IC(50) values be

244 -3 (MMP-3) was lower in CAFs but elevated in prostate cancer cells relative to their normal counterpa

245 ution into castration or therapy resistance, prostate cancer cells reprogram the androgen responses t

246 roach provides a better understanding of how prostate cancer cells respond heterogeneously to androge

247 proliferative arrest and differentiation of prostate cancer cells, responses not elicited when POLR3

248 Overexpression of RBMS1 in DU145 and LNCaP prostate cancer cells resulted in diminished cell prolif

249 Knockdown of SUB1 in prostate cancer cells resulted in reduced cell prolifera

250 easuring inhibition of ephrin-A1-induced PC3 prostate cancer cell retraction.

251 t ETV1 may enhance TGF-beta signaling in PC3 prostate cancer cells, revealing a different facet of th

252 nted here comprised either melanoma cells or prostate cancer cells stably adorned with Toll-like rece

253 hat MYC plays an important role in promoting prostate cancer cell survival.

254 tudy, we investigated the role of miR-214 on prostate cancer cell survival/migration/invasion, cell c

255 and simultaneous Cai2+ imaging in mammalian prostate cancer cells that an early step in the signal c

256 We demonstrate that prostate cancer cells that are insensitive to ADT, as we

257 e gene transcription or DNA-damage repair in prostate cancer cells that co-express AR-V7 and AR-FL.

258 inase A (AURKA) is regulated by androgens in prostate cancer cells that express high levels of AR.

259 ression of AURKA is regulated by androgen in prostate cancer cells that highly express AR, emphasizin

260 Importantly, the polymer killed dormant prostate cancer cells that were resistant to docetaxel.

261 Here we show, in prostate cancer cells, that LSD1 associates with FOXA1 a

262 l domain to sequester AR in the cytoplasm of prostate cancer cells, thereby reducing AR transcription

263 kdown of EAF2 or its homolog EAF1 sensitized prostate cancer cells to DNA damage and the sensitizatio

264 al complex, contributing to sensitization of prostate cancer cells to enzalutamide treatment.

265 ed combined ChIP-seq and RNA-seq analyses of prostate cancer cells to identify direct ZBTB7A-represse

266 EK5 knockdown by RNA interference sensitizes prostate cancer cells to ionizing radiation (IR) and eto

267 cell debris allow macropinocytic breast and prostate cancer cells to proliferate, despite fatty acid

268 tablished that galectin-4 expression enabled prostate cancer cells to repopulate tumors in orthotopic

269 that RAGE-PR3 interaction mediates homing of prostate cancer cells to the bone marrow.

270 l lines, and that a depletion of Ate1 drives prostate cancer cells towards more aggressive pro-metast

271 xenografts were established using aggressive prostate cancer cells transduced with miR-23b/-27b or no

272 transcriptome profiling of 144 single LNCaP prostate cancer cells treated or untreated with androgen

273 Optical imaging of DU-145 prostate cancer cells treated with corrole NPs (<=100 nM

274 We further show that prostate cancer cells use alphav integrin to migrate eff

275 ion chromatin interaction maps in normal and prostate cancer cells using in situ Hi-C.

276 r suspension, induced a phenotypic switch in prostate cancer cells via mechanotransduction.

277 alpha represses the metastatic properties of prostate cancer cells via modulation of the polyamine bi

278 lators can be used to suppress AR/ARV-driven prostate cancer cells via regulation of pharmacologicall

279 notransduction-mediated phenotypic switch in prostate cancer cells was accompanied by decreased sensi

280 astasis, ectopic expression of RAGE on human prostate cancer cells was sufficient to promote bone mar

281 The mechanosensitive phenotypic switching in prostate cancer cells was sustainable yet reversible eve

282 ne tumor growth in which apoptosis-inducible prostate cancer cells were either coimplanted with verte

283 a, 4T1 mouse breast cancer, and DU 145 human prostate cancer cells were used as clinical models.

284 und this isoform to be strongly expressed in prostate cancer cells, where it displayed an enhanced au

285 prostate to be used as individual markers of prostate cancer cells, whereas others could be truly pro

286 ng and more aggressive invasive character in prostate cancer cells, which through better survival in

287 erformed in vitro revealed that treatment of prostate cancer cells with 27-hydroxycholesterol (27HC),

288 parate polystyrene microbeads and PC-3 human prostate cancer cells with 94.7 and 1.2% of the cells an

289 Sustained treatment of prostate cancer cells with androgens increased the activ

290 Genetically rescuing WNT3A levels in prostate cancer cells with endogenously blocked TBX2 par

291 Treatment of prostate cancer cells with enzalutamide enhances recruit

292 rrent in vitro study shows that treatment of prostate cancer cells with goserelin-conjugated gold nan

293 Treatment of CAFs but not prostate cancer cells with hydrogen peroxide directly in

294 drogen receptor (AR) locus is altered in the prostate cancer cells with many cancer-specific enhancer

295 We report that breast and prostate cancer cells with mutant p53 respond to insulin

296 cterized the plasticity and heterogeneity of prostate cancer cells with regard to androgen dependence

297 we compared the entire transcriptome of PC3 prostate cancer cells with those cells in which GNA13 ex

298 Treatment of highly invasive breast and prostate cancer cells with WAHM inhibitor peptides signi

299 anti-invasive and antitumor effects against prostate cancer cells, with minimal toxic side-effects i

300 ue from mice bearing miR-23b/-27b-transduced prostate cancer cell xenografts compared with scrambled