ライフサイエンスコーパス: prostate cancer cell

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

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

3 23b/-27b-mediated repression of migration in prostate cancer cells.

4 nd hindered tumorigenicity of radioresistant prostate cancer cells.

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

6 nd inhibits skeletal metastasis formation of prostate cancer cells.

7 in reactivation of transposable elements in prostate cancer cells.

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

9 e MMP9 and promoted the metastatic growth of prostate cancer cells.

10 phenotype and increases the invasiveness of prostate cancer cells.

11 PRMT5 is restricted to TMPRSS2:ERG-positive prostate cancer cells.

12 to be active in reducing the growth of LNCaP prostate cancer cells.

13 t CRL3(SPOP)-dependent degradation of ERG in prostate cancer cells.

14 ndependent mechanism in castration-resistant prostate cancer cells.

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

16 vated levels of active phosphorylated AKT in prostate cancer cells.

17 mal human mammary epithelial cells and LNCaP prostate cancer cells.

18 CRPC and enzalutamide-resistant phenotype in prostate cancer cells.

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

20 thway is activated in enzalutamide-resistant prostate cancer cells.

21 membrane antigen (PSMA) to deliver (125)I to prostate cancer cells.

22 riptionally suppress both PTEN and PTENP1 in prostate cancer cells.

23 ATM-mediated DDR signaling in AR-inactivated prostate cancer cells.

24 n prostate cancer increases the migration of prostate cancer cells.

25 ith the invasive growth and dissemination of prostate cancer cells.

26 Siah2-dependent regulation of AR activity in prostate cancer cells.

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

28 ding to distinct transcriptional outcomes in prostate cancer cells.

29 egulates the expression of c-Myc oncogene in prostate cancer cells.

30 cytosolic and nuclear beta-catenin in human prostate cancer cells.

31 by the inhibition of luciferase refolding in prostate cancer cells.

32 verexpression leads to a growth advantage of prostate cancer cells.

33 LC2) in intact human breast, lung, colon and prostate cancer cells.

34 g TGFbeta receptor II (TGFBR2) expression in prostate cancer cells.

35 ctor that regulates the behavior and fate of prostate cancer cells.

36 transduction-induced phenotypic switching of prostate cancer cells.

37 and invasion through Matrigel of benign and prostate cancer cells.

38 outgrowth of distant and otherwise indolent prostate cancer cells.

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

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

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

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

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

44 -1beta and IL-18 were confined to aggressive prostate cancer cells.

45 tively controls mitochondrial respiration in prostate cancer cells.

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

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

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

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

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

51 TGF-beta upregulates in prostate cancer cells a set of genes associated with can

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

53 In breast and prostate cancer cells, AFAP1 has been shown to regulate

54 PIP and PSMA-negative (PSMA-) PC3 flu human prostate cancer cells after treatment with (125)I-DCIBzL

55 important role in the survival and growth of prostate cancer cells, although details of the underlyin

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

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

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

59 y affects the viability of Myc-overactivated prostate cancer cells and completely blocks their invasi

60 f the Plk1 inhibitor BI2536 in both cultured prostate cancer cells and CRPC xenograft tumors.

61 d USP9X as a potential therapeutic target in prostate cancer cells and established WP1130 as a lead c

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

63 d cell migration of human C4-2B4 and PC3-mm2 prostate cancer cells and human HEK293T cells.

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

65 a transforming oncogene widely expressed in prostate cancer cells and maintains their transformed ph

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

67 alloproteinase 2 (MMP2) in vitro in multiple prostate cancer cells and promotes osteolysis in vivo in

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

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

70 Prostate cancer cells and secreted prostasomes expose lo

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

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

73 eration and viability of glioma, breast, and prostate cancer cells and v-Src-transformed murine fibro

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

75 tor (AR) signaling is a critical pathway for prostate cancer cells, and androgen-deprivation therapy

76 ed using cultured prostate epithelial cells, prostate cancer cells, and HEK-293 cells stably expressi

77 c properties of these agents in solution, in prostate cancer cells, and in an in vivo experimental mo

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

79 store-operated Ca(2+) channels in hPECs and prostate cancer cells are heteromeric Orai1/Orai3 channe

80 a role in maintaining telomere stability in prostate cancer cells, as AR inactivation induces telome

81 Ectopic expression of Wnt5a in prostate cancer cells attenuates the antiproliferative e

82 te the effects of bupivacaine on ovarian and prostate cancer cell biology and the underlying molecula

83 that CDK5 acts as a crucial signaling hub in prostate cancer cells by controlling androgen responses

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

85 we report a profound effect of endostatin on prostate cancer cells by efficient intracellular traffic

86 a growth factor, leading to proliferation of prostate cancer cells by promoting insulin-like response

87 sults, knockdown of ATF3 expression in human prostate cancer cells by single guided RNA-mediated targ

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

89 ble chemical extraction of whole nuclei from prostate cancer cells captured using geometrically enhan

90 xtracellular Hsp90 (eHsp90) initiates EMT in prostate cancer cells, coincident with its enhanced expr

91 highly upregulated in enzalutamide-resistant prostate cancer cells compared to the parental cells.

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

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

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

95 , we found that Siah2 inhibition in CWR22Rv1 prostate cancer cells decreased AKR1C3 expression as wel

96 PRUNE2 expression or silencing in prostate cancer cells decreased and increased cell proli

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

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

99 sponses in primary human prostate cells, PC3 prostate cancer cells, dorsal root ganglion neurons, and

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

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

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

103 The recovery of prostate cancer cells (DU145) spiked into whole blood wa

104 Also, human prostate cancer cells, DU145 and PC-3, knocked down for

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

106 induced binding of androgen receptor (AR) to prostate cancer cell enhancers as a model, we show rapid

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

108 In addition, in human luminal-type prostate cancer cells, ERG binds to the promoter of YAP1

109 alpha2M*-treated human prostate cancer cells exhibit a 2-3-fold increase in glu

110 duction in ovarian, lung, colon, breast, and prostate cancer cells exposed to three other structurall

111 Furthermore, we determined that prostate cancer cells express high levels of CTR1, the p

112 ed that miR-34a levels were reduced in CD44+ prostate cancer cells (Figure 1B).

113 miR-221 expression sensitized prostate cancer cells for IFN-gamma-mediated growth inhi

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

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

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

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

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

119 en to identify signaling pathways regulating prostate cancer cell growth led to our discovery that ch

120 as was NEDD9's potential biological role in prostate cancer cell growth regulation.

121 MiR-190a contributes the human prostate cancer cell growth through AR-dependent signali

122 Here we demonstrate that AR regulates prostate cancer cell growth via the metabolic sensor 5'-

123 therapy because androgens are essential for prostate cancer cell growth.

124 suppresses AR-dependent gene expression and prostate cancer cell growth.

125 d gene-specific HIF-dependent expression and prostate cancer cell growth.

126 ah2 enhanced AR transcriptional activity and prostate cancer cell growth.

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

128 However, prostate cancer cells in advanced stages become resistan

129 t study, we developed enzalutamide-resistant prostate cancer cells in an effort to understand the mec

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

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

132 miR-124 inhibited proliferation of prostate cancer cells in vitro and sensitized them to in

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

134 ted the cell surface of androgen-independent prostate cancer cells in vitro, and homed to androgen re

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

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

137 NQO1 silencing in prostate cancer cells increased levels of nuclear IKKalp

138 Knockdown of PFKFB4 in prostate cancer cells increased p62 and reactive oxygen

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

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

141 of liposomes were evaluated on monolayers of prostate cancer cells intrinsically expressing PSMA (hum

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

143 lytic cascade that mediates androgen-induced prostate cancer cell invasion, tumor growth, and metasta

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

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

146 induces an initial Ca(2+) increase, which in prostate cancer cells is blocked at high concentrations

147 cate that the oncogenic function of c-Myc in prostate cancer cells is regulated by 5-Lox activity, re

148 34a and chemosensitizes paclitaxel-resistant prostate cancer cells, killing both cancer stem-like cel

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

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

151 A prostate cancer cell line (PC3) immobilized on an atomic

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

153 ll lines PANC-1 and MIAPaCa-2 as well as the prostate cancer cell line DU145.

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

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

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

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

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

159 o, eHsp90 secretion was stably enforced in a prostate cancer cell line resembling indolent disease.

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

161 anscriptional and epigenetic regulators in a prostate cancer cell line, LNCaP-abl.

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

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

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

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

166 F-1alpha signaling pathways were examined in prostate cancer cell lines (LNCaP, 22Rv1) with assays me

167 helial cells (hPECs) from healthy tissue and prostate cancer cell lines (LNCaP, DU145, and PC3).

168 androgen-insensitive and androgen-sensitive prostate cancer cell lines and an aggressive cervical ca

169 olorectal tumors as well as CRC, breast, and prostate cancer cell lines and associated with a mesench

170 Metastatic prostate cancer cell lines and bone metastasis samples d

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

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

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

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

175 es revealed that overexpression of miR-25 in prostate cancer cell lines and selected subpopulation of

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

177 7A1, reduced cellular cholesterol content in prostate cancer cell lines by inhibiting the activation

178 Prostate cancer cell lines derived from HiMyc tumors (HM

179 Knockdown of DDX3 in the aggressive prostate cancer cell lines DU145 and 22Rv1 resulted in s

180 RK-33 treatment of prostate cancer cell lines DU145, 22Rv1, and LNCaP (whic

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

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

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

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

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

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

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

188 diting, we created a panel of isogenic 22Rv1 prostate cancer cell lines representing all three genoty

189 daurus to (i) integrate epigenetic data from prostate cancer cell lines to validate the activation fu

190 Western blot experiments with four different prostate cancer cell lines treated with KU675 supported

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

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

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

194 the growth and tumorigenic capacity of human prostate cancer cell lines, but enhances migratory capac

195 rug activated by ROS was demonstrated in two prostate cancer cell lines, LNCaP and DU-145.

196 In prostate cancer cell lines, recombinant LOX-PP (rLOX-PP)

197 bisulfite sequencing dataset generated from prostate cancer cell lines, we have shown that BSPAT is

198 Using rapidly dividing human prostate cancer cell lines, we identified mitotically qu

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

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

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

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

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

204 inhibit proliferation in androgen-dependent prostate cancer cell lines.

205 K5 is necessary for proliferation of several prostate cancer cell lines.

206 growth in a panel of enzalutamide resistant prostate cancer cell lines.

207 in both androgen-dependent and -independent prostate cancer cell lines.

208 s, but enhances migratory capacities of some prostate cancer cell lines.

209 were present in 22Rv1, LNCaP, and VCaP human prostate cancer cell lines.

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

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

212 mRNA was upregulated in androgen-insensitive prostate cancer cells (LNCaP-C81 and LNCaP-C4-2 cells) c

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

214 S-induced alterations in Ca(2+) signaling in prostate cancer cells may contribute to the higher sensi

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

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

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

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

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

220 ults identify YAP to be a novel regulator in prostate cancer cell motility, invasion, and castration-

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

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

223 Animals injected with human fibroblasts, prostate cancer cells, or collagen served as control ani

224 These events may render prostate cancer cells particularly sensitive to inhibiti

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

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

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

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

229 that neuroendocrine transdifferentiation in prostate cancer cell populations influences the progress

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

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

232 ty in PC tumor tissues, while not inhibiting prostate cancer cell proliferation from the MTT assay an

233 iR-23b/-27b expression or inhibition impacts prostate cancer cell proliferation suggesting that miR-2

234 and as a major driver of androgen-dependent prostate cancer cell proliferation.

235 -3 (MMP-3) was lower in CAFs but elevated in prostate cancer cells relative to their normal counterpa

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

237 namic regulation of Rad51 by E2F1 and p53 in prostate cancer cells' response to hypoxia and DNA damag

238 ion by gamma-tocopherol (2) in PTEN-negative prostate cancer cells resulted from its unique ability t

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

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

241 sion of BMI1 in MCF7 breast cancer and DU145 prostate cancer cells significantly reduced ETOP-induced

242 In prostate cancer cells, SOCE is blocked at lower concentr

243 In prostate cancer cells, SRC-2 stimulated reductive carbox

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

245 We show here that irradiating prostate cancer cells stimulates a durable upregulation

246 gically or genetically significantly impairs prostate cancer cell survival in vitro and in vivo, impl

247 effective in cell lysates, more cytotoxic in prostate cancer cells than 3a and potentiates the cytoto

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

249 is study aimed to identify subpopulations of prostate cancer cells that are responsible for the initi

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

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

252 lso found that restoration of OLFM4 in human prostate-cancer cells that lack OLFM4 expression signifi

253 In prostate cancer cells, the gene expression of AR targets

254 Gene expression profiling of prostate cancer cells, their radioresistant derivatives,

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

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

257 methacin resensitized enzalutamide-resistant prostate cancer cells to enzalutamide treatment both in

258 e a suitable microenvironment for ALDH(high) prostate cancer cells to establish metastatic growths, o

259 Given the propensity of prostate cancer cells to form bone metastatic lesions, w

260 ostate cancer and involved in the ability of prostate cancer cells to induce axonogenesis.

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

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

263 eracts with DNA repair proteins to sensitize prostate cancer cells to the effects of ionizing radiati

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

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

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

267 re quantified in large numbers of individual prostate cancer cells using large area synchrotron X-ray

268 otes the growth, invasion, and metastasis of prostate cancer cells via matriptase activation and extr

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

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

271 Our results indicate iAs may enhance prostate cancer cell viability through a previously unre

272 e outputs indicating a significant impact on prostate cancer cell viability, osteoclast formation and

273 ected after 1 week of iAs exposure increased prostate cancer cell viability, whereas CM from ASCs tha

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

275 ed monolayer (2D) and multilayer (3D) DU-145 prostate cancer cells was higher than that of control gr

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

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

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

279 that membrane surface E-cadherin-expressing prostate cancer cells were resistant to cell death by ch

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

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

282 y shown to function as a tumor suppressor in prostate cancer cells, where its expression correlated w

283 the speed and directionality of migration of prostate cancer cells, which is consistent with an obser

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

285 rane antigen (PSMA) is overexpressed in most prostate cancer cells while being present at low or unde

286 ty to selectively deliver cytotoxic drugs to prostate cancer cells while sparing normal cells that la

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 is significantly affected by pretreatment of prostate cancer cells with fatostatin A, which blocks st

292 We treated 22Rv1 prostate cancer cells with fractionated 2 Gy radiation t

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

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

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 chanism to target the AR(-/lo) population of prostate cancer cells with stem-cell properties.

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