ライフサイエンスコーパス: prostate cancer cell line

1 ion factors, is occupied by FOXA1 in a human prostate cancer cell line.

2 3, and cleaved caspase 3 in the LNCaP human prostate cancer cell line.

3 of AKT phosphorylation by GRP78 knockdown in prostate cancer cell line.

4 cell lines and the hormone-insensitive PC-3 prostate cancer cell line.

5 ssion promoted colony formation in the 22Rv1 prostate cancer cell line.

6 rentiation in DU145, an androgen-independent prostate cancer cell line.

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

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

9 studies were performed using the human PC-3 prostate cancer cell line.

10 nished growth and migration of an aggressive prostate cancer cell line.

11 ports the effects of rBbKIm on DU145 and PC3 prostate cancer cell lines.

12 status and PDGF isoforms were noted in human prostate cancer cell lines.

13 se increased glycan expression on breast and prostate cancer cell lines.

14 PIAS1 was observed in the majority of tested prostate cancer cell lines.

15 roliferation and colony formation ability of prostate cancer cell lines.

16 vels as a function of progressively invasive prostate cancer cell lines.

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

18 cell viability assays against PC-3 and LNCaP prostate cancer cell lines.

19 correlated with promoter DNA methylation in prostate cancer cell lines.

20 ounds also inhibit growth in human and mouse prostate cancer cell lines.

21 f CARM1 inhibits proliferation of breast and prostate cancer cell lines.

22 n syndrome, is highly elevated in metastatic prostate cancer cell lines.

23 prostate (TRAMP) mice as well as in vitro in prostate cancer cell lines.

24 NCaP) and androgen-insensitive (DuPro) human prostate cancer cell lines.

25 ic and osteoblastic lesions induced by human prostate cancer cell lines.

26 of inducing cell cycle progression in human prostate cancer cell lines.

27 uinol-mediated proteasome inhibition in both prostate cancer cell lines.

28 ier expression in human prostate tumours and prostate cancer cell lines.

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

30 ificant number of breast, ovarian, liver and prostate cancer cell lines.

31 CaP prostate cancer cell line, but not other prostate cancer cell lines.

32 ated in mitoxantrone and docetaxel-resistant prostate cancer cell lines.

33 pressed the expression of RKIP in metastatic prostate cancer cell lines.

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

35 cancer cell lines (MCF-7, HCC1937) and three prostate cancer cell lines.

36 a cells but was absent in metastases-derived prostate cancer cell lines.

37 ound polysomal mRNA prepared from breast and prostate cancer cell lines.

38 d cellular location of R11 in four different prostate cancer cell lines.

39 nt (LNCaP) and -independent (DU145 and PC-3) prostate cancer cell lines.

40 human (LNCaP) and mouse (TRAMP-C1A and -C2H) prostate cancer cell lines.

41 primary human and mouse prostate cancers and prostate cancer cell lines.

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

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

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

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

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

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

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

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

50 lidation rate (94%) in an RNA-Seq dataset of prostate cancer cell lines.

51 in vivo and in isogenic oncogene-transformed prostate cancer cell lines.

52 ity against LNCaP and enzalutamide-resistant prostate cancer cell lines.

53 he development of CRPC phenotype in multiple prostate cancer cell lines.

54 ype-specific phosphorylation was observed in prostate cancer cell lines.

55 ncy against LNCaP and Enzalutamide-resistant prostate cancer cell lines.

56 pression of NuSAP in the LNCaP and PC3 human prostate cancer cell lines.

57 ial activation in prostate epithelial versus prostate cancer cell lines.

58 7 expression and androgen glucuronidation in prostate cancer cell lines.

59 as well as xenografts derived from the human prostate cancer cell line 22Rv1 that naturally express A

60 DU-145, PC-3, and CWR22Rv.1 prostate cancer cell lines (a total of 1 x 10(6) cells)

61 From screening of several CPPs in prostate cancer cell lines, a polyarginine peptide (R11)

62 sing in vitro activity toward five different prostate cancer cell lines, all representative of CPRC a

63 CDK5 in the highly metastatic Dunning AT6.3 prostate cancer cell line also greatly impaired invasive

64 Other IL-8-expressing prostate cancer cell lines also exhibited similar phenot

65 In human prostate cancer cell lines, although not in the mouse mo

66 cell line and normal tissues, but not in the prostate cancer cell line and eight primary prostate can

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

68 ssing FOXA1 in the androgen-responsive LNCaP prostate cancer cell line and observed a significant inc

69 ll line and the TMPRSS2-ERG gene fusion in a prostate cancer cell line and tissues.

70 Several prostate cancer cell lines and a subset of primary prost

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

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

73 Metastatic prostate cancer cell lines and bone metastasis samples d

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

75 Importantly, Rad9 is up-regulated in prostate cancer cell lines and clinical specimens.

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

77 orrelates with metastatic phenotypes in both prostate cancer cell lines and human prostate cancer spe

78 aracterizing RREB1 expression in bladder and prostate cancer cell lines and human tissue samples.

79 NCaP) and tested on independent data sets of prostate cancer cell lines and human tumors to assess it

80 LNCaP) and castration-resistant (ie, C4-2B) prostate cancer cell lines and in cells isolated from a

81 target for gallium complexes in a variety of prostate cancer cell lines and in human prostate cancer

82 icroarrays to identify AR-regulated genes in prostate cancer cell lines and in prostate tumours, we p

83 inhibited colony formation in LNCaP and PC3 prostate cancer cell lines and inducible expression of D

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

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

86 he mechanism underlying TIMP-2 expression in prostate cancer cell lines and primary prostate tumor sa

87 und that GLI2 protein is expressed highly in prostate cancer cell lines and primary tumors, whereas t

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

89 of 17- to 26-base-long RNAs was created from prostate cancer cell lines and sequenced by ultra-high-t

90 we report that LOX expression is reduced in prostate cancer cell lines and that recombinant LOX-PP p

91 gma expression is lost in LNCaP and Tramp-C1 prostate cancer cell lines and that this expression is r

92 A methylation status of the rDNA promoter in prostate cancer cell lines and the clinical specimens.

93 ated the expression of SSX family members in prostate cancer cell lines and tumor biopsies to identif

94 m of ERK), inhibited cell growth in cultured prostate cancer cell lines and tumor growth particularly

95 we show that C17orf37 is highly expressed in prostate cancer cell lines and tumors, compared to minim

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

97 Complement deposition on Du145 cells (human prostate cancer cell line) and anti-MUC1 mAb-mediated co

98 rogen-regulated gene expression in the LNCaP prostate cancer cell line, and identifies a number of an

99 ty, is expressed in a panel of human and rat prostate cancer cell lines, and is also expressed in 87.

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

101 r were targets of proliferative signaling in prostate cancer cell lines, and that cyclin D1 was requi

102 that Ron is overexpressed in PC-3 and DU145 prostate cancer cell lines, and that the levels of angio

103 C1 interaction in human prostate tissues, in prostate cancer cell lines, and with purified maspin.

104 re tested for cytotoxicity against two human prostate cancer cell lines, androgen-dependent LNCaP and

105 MAT-LyLu, as well as two human nonmetastatic prostate cancer cell lines, androgen-dependent LnCaP and

106 We determined that, in human prostate cancer cell lines, ARv567es functioned as a con

107 rexpressed in both AR-positive and -negative prostate cancer cells lines, as well as in 50% (10 of 20

108 ositive (LNCaP) and -negative (PC-3, DU-145) prostate cancer cell lines associated with an increase o

109 TREK-1 is highly expressed in PC3 and LNCaP prostate cancer cell lines but is not detectable in norm

110 hibited tumor cell growth in all transformed prostate cancer cell lines but not PrEC cells.

111 ma cells, breast cancer cells, and the LNCaP prostate cancer cell line, but not other prostate cancer

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

113 lates Kaiso at the RNA and protein levels in prostate cancer cell lines, but more interestingly cause

114 y, a subset of these chimeras was present in prostate cancer cell lines, but not detectable in primar

115 cell proliferation of 22Rv1, LNCaP, and VCaP prostate cancer cell lines by 70%, 61%, and 20%, respect

116 tumorigenicity and invasiveness of multiple prostate cancer cell lines by cyclic AMP-dependent prote

117 n shown to exhibit antineoplastic effects in prostate cancer cell lines by induction of cell cycle ar

118 7A1, reduced cellular cholesterol content in prostate cancer cell lines by inhibiting the activation

119 We show CDCP1 expression on prostate cancer cell lines by real-time quantitative PCR

120 lly, reduction of eIF3h levels in breast and prostate cancer cell lines by short interfering RNA meth

121 es of androgen receptor-positive (AR+) human prostate cancer cell lines, CD133+ cells are present at

122 agic form of cell death in colon, breast and prostate cancer cell lines, characterized by extensive c

123 that KLF4 is significantly downregulated in prostate cancer cell lines compared with nontumorigenic

124 sion of miR-331-3p and miR-642-5p in several prostate cancer cell lines compared with normal prostate

125 detected in nuclear fractions among several prostate cancer cell lines, compared to normal prostate

126 Similarly, murine prostate cancer cell lines containing a Ron deficiency e

127 ivation in the presence of androstanediol in prostate cancer cell lines correlated mainly with mRNA a

128 We found that four prostate cancer cell lines (CWR22, DU145, LNCaP, and PC-

129 We studied human prostate cancer cell lines CWR22Rv1 and CWR-R1, which pr

130 c-Met expression in an androgen-insensitive prostate cancer cell line, CWR22Rv1.

131 vity at low levels of androgen in the CWR-R1 prostate cancer cell line derived from the castration-re

132 ding domain (ARVs), originally isolated from prostate cancer cell lines derived from a single patient

133 Prostate cancer cell lines derived from HiMyc tumors (HM

134 und that the aggressive LN3, C4-2, and C4-2B prostate cancer cell lines derived from LNCaP possess co

135 treatment-naive primary prostate tissue and prostate cancer cell line-derived xenografts.

136 of Galpha12 or Galpha13 in the PC3 and DU145 prostate cancer cell lines did not promote cancer cell g

137 Knockdown of PTK6 in the PC3 human prostate cancer cell line disrupts FAK and AKT activatio

138 The same was also true for the prostate cancer cell line DU-145 (but not for normal PZ-

139 In a prostate cancer cell line DU145 lacking functional EphB2

140 resumptive catalytically dead mutant) in the prostate cancer cell line DU145 resulted in decreased co

141 XMRV replication in the prostate cancer cell line DU145 was sensitive to inhibit

142 n inhibited triterpenoid-mediated killing of prostate cancer cell line Du145, suggesting that the int

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

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

145 Forced overexpression of GPx3 in prostate cancer cell lines DU145 and PC3 as well as immo

146 Forced expression of CSR1 in prostate cancer cell lines DU145 and PC3 resulted in a t

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

148 olunteers spiked with tumor cells from three prostate cancer cell-lines (DU145, PC3, LNCaP).

149 stasis of a tumorigenic, nonmetastatic human prostate cancer cell line, DU145.

150 In this study, we use the human prostate cancer cell lines, DU145 and PC3, to investigat

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

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

153 In prostate cancer cell lines, FTY720 acted as a sphingosin

154 ploited the mifepristone-induced SRC-3 LNCaP prostate cancer cell line generated in our laboratory to

155 Herein, murine prostate cancer cell lines, generated via selective tran

156 accurately predicts AR activity in multiple prostate cancer cell lines, has minimal variation betwee

157 based motility and migration in a metastatic prostate cancer cell line (i.e., PC-3) without disruptin

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

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

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

161 steolytic, and mixed lesions formed by human prostate cancer cell lines in a severe combined immunode

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

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

164 of podocalyxin in MCF7 breast cancer and PC3 prostate cancer cell lines increased their in vitro inva

165 ncentrations of dihydrotestosterone (DHT) to prostate cancer cell lines increases translation of endo

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

167 Analyses of Nkx3.1 knockout mice and human prostate cancer cell lines indicate that NKX3.1 represse

168 Overexpression of GPx3 in prostate cancer cell lines induced the suppression of co

169 In both DU-145 and PC-3 prostate cancer cell lines, Kaiso inhibition (short hair

170 egulates functional alphaDG glycosylation in prostate cancer cell lines; knockdown of LARGE2 resulted

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

172 itonin-calcitonin receptor autocrine loop in prostate cancer cell lines led to the loss of cell-cell

173 gnificantly inhibited the viability of human prostate cancer cell line LNCaP (androgen-dependent) and

174 he antibody does not detect a protein in the prostate cancer cell line LNCaP, which has very low NGEP

175 eomic profile of the poorly metastatic human prostate cancer cell line LNCaP, with its highly metasta

176 al human breast cancer cell lines and in the prostate cancer cell line LNCaP.

177 ed ID1 upregulation was recapitulated in the prostate cancer cell line LNCaP.

178 DU 145 compared with the androgen-dependent prostate cancer cell line LNCaP.

179 tracellular localization and function in the prostate cancer cell line LNCaP.

180 293T cells overexpressing the AR and in the prostate cancer cell line LNCaP.

181 tenuates the androgen-mediated growth of the prostate cancer cell line LNCaP.

182 horylation, using mutated Stat3 in the human prostate cancer cell line LNCaP.

183 pic model of prostate cancer using the human prostate cancer cell line LNCaP.

184 ent-dependent cytotoxicity (CDC) against the prostate cancer cell line LNCap.

185 es as antiandrogens were tested in the human prostate cancer cell line LNCaP.

186 examined the biological properties of human prostate cancer cell lines LNCaP and PC-3, in which oste

187 verse sialylation activity is noted in human prostate cancer cell lines LNCaP and PC3.

188 Suppression of AIF expression in the prostate cancer cell lines LNCaP, DU145, and PC3 demonst

189 ompared with those in the androgen-dependent prostate cancer cell line (LNCaP).

190 ease (SENP1) in the androgen-sensitive human prostate cancer cell line (LNCaP).

191 Prostate cancer cell lines (LNCaP and DU-145) had increa

192 Here we showed, using two prostate cancer cell lines (LNCaP and PC-3) and primary

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

194 requency in recurrent prostate cancer and in prostate cancer cell lines (LNCaP, CWR22, PC3, and DU145

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

196 was observed in human prostate cancer, human prostate cancer cell lines (LNCaP, DU145, PC3, and CW22r

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

198 In the Pten-deficient prostate cancer cell line, LNCaP, restoration of Pten wa

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

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

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

202 AR expression in the two androgen-sensitive prostate cancer cell lines, LNCaP and LAPC4, significant

203 errant activation of ETV1, we identified two prostate cancer cell lines, LNCaP and MDA-PCa 2B, that h

204 concentrations induce apoptosis of cultured prostate cancer cell lines, LNCaP, ALVA31, Du145, PC3, a

205 possibility was tested by using the AS human prostate cancer cell lines, LNCaP, CWR22Rv1, and LAPC-4.

206 In this investigation, we studied four human prostate cancer cell lines, LNCaP, DU145, LAPC4, and PC3

207 n this study, we used the androgen-dependent prostate cancer cell line MDA PCa 2b, derived from a hum

208 The prostate cancer cell lines metastasized in FVB mice to b

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

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

211 Reconstitution of miR-708 in prostate cancer cell lines or CD44(+) prostate cancer ce

212 erexpression of p45-sErbB3 in the osteolytic prostate cancer cell line PC-3 converted its phenotype f

213 The human prostate cancer cell line PC-3 was used to determine the

214 cal intensity, while the strongly metastatic prostate cancer cell line PC-3-M migrates anodally.

215 suppresses the in vivo tumorigenicity of the prostate cancer cell line PC-3.

216 iferative effects of adaphostin in the human prostate cancer cell line PC-3.

217 amples and in the human androgen-independent prostate cancer cell lines PC-3 and DU 145 compared with

218 lated compounds on the decreased survival of prostate cancer cell lines PC-3, DU-145, and LNCaP by in

219 Depletion of FoxM1 levels in prostate cancer cell lines PC-3, LNCaP, or DU-145 by sma

220 In the human prostate cancer cell line, PC-3, delivery of exogenous n

221 gy to down-regulate ADAM15 in the metastatic prostate cancer cell line, PC-3.

222 ce the cytotoxic effects of radiation on two prostate cancer cell lines, PC-3 and DU145.

223 lly, the osteosarcoma cell line U2OS and the prostate cancer cell line PC3 (p14(ARF)-deficient and p5

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

225 growth inhibitory effects against the human prostate cancer cell line PC3 at submicromolar concentra

226 We also show that growth of the prostate cancer cell line PC3 is inhibited by the treatm

227 ostate cancer cells, we established a stable prostate cancer cell line PC3 with CYP24A1 promoter driv

228 s (large cell lung cancer cell line H460 and prostate cancer cell line PC3) were given bevacizumab ve

229 analyses with the glycolipid extract of the prostate cancer cell line PC3, microarrays with sequence

230 In a human prostate cancer cell lines PC3 (p53(null)), curcumin red

231 sion of ITGA7 induced apoptosis in the human prostate cancer cell lines PC3 and DU145.

232 d for investigating the androgen-independent prostate cancer cell lines PC3 and DU145.

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

234 ied by partial knockdown of STAT1 in a human prostate cancer cell line (PC3), suggesting that this pa

235 igher levels in several androgen-independent prostate cancer cell lines (PC3, DU145, cds1, cds2, and

236 We show that prostate cancer cell lines (PC3, LNCaP and DU145), but n

237 a breast epithelial cell line, MCF10A, and a prostate cancer cell line, PC3.

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

239 t or Erk signaling in an androgen-responsive prostate cancer cell line promotes hormone-independent b

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

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

242 osine levels were also increased in invasive prostate cancer cell lines relative to benign prostate e

243 were downregulated in all assays in advanced prostate cancer cell lines relative to the parental cell

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

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

246 the less aggressive androgen-dependent LNCaP prostate cancer cell line resulted in enhanced invasion

247 iated myosin VI knockdown in the LNCaP human prostate cancer cell line resulted in impaired in vitro

248 23b/-27b in metastatic, castration-resistant prostate cancer cell lines resulted in a significant att

249 -27b in two independent castration-resistant prostate cancer cell lines resulted in suppression of in

250 Biochemical analysis of prostate cancer cell lines reveals that ALCAM expression

251 mal prostate epithelial cells (PrEC) and the prostate cancer cell lines RWPE-1, WPE1-NA22, WPE1-NB14,

252 Recent biochemical data suggest that human prostate cancer cell lines show a redox imbalance (oxidi

253 studies of these analogues in PC3 and LNCaP prostate cancer cell lines showed that the analogues are

254 while both Src and Abl are expressed in all prostate cancer cell lines, Src but not Abl is activated

255 urified from the conditioned medium of human prostate cancer cell lines, stimulated growth and enhanc

256 geting these lncRNAs in castration-resistant prostate cancer cell lines strongly suppressed tumour xe

257 interfering RNA induced apoptosis in all the prostate cancer cell lines studied.

258 cer progresses and is minimal in established prostate cancer cell lines such as PC-3, DU-145, and LNC

259 Deficient DNA repair was dependent on the prostate cancer cell line tested, suggesting a complex p

260 and signal pathway of VIP in LNCaP cells, a prostate cancer cell line that requires androgens for gr

261 expression patterns between two bone-derived prostate cancer cell lines that produce osteoblastic (MD

262 The generation of new oncogene-specific prostate cancer cell lines that recapitulate human prost

263 In the PC3 prostate cancer cell line, the pool of endogenous activa

264 osure of apoptosis-resistant renal, lung and prostate cancer cell lines to ABT-737, although not capa

265 In this study, we use prostate cancer cell lines to test the hypothesis that r

266 In vitro studies were done on a panel of prostate cancer cell lines to understand the molecular b

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

268 cell-cycle regulators were observed in human prostate cancer cell lines, transiently transfected with

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

270 y profiling of the androgen-responsive LNCaP prostate-cancer cell line treated with R1881 for the ide

271 assessed using the BB2r-positive PC-3 human prostate cancer cell line under hypoxic and normoxic env

272 tion site) is present in the most aggressive prostate cancer cell lines, unexpectedly high phosphoryl

273 d 14-3-3sigma gene expression in a subset of prostate cancer cell lines using methylation-specific PC

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

275 By stably transfecting PSA cDNA into various prostate cancer cell lines, we found that PSA could prom

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

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

278 Using xenografts propagated from human prostate cancer cell lines, we reveal that nuclear PTEN

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

280 Prostate cancer cell lines were examined for proteins th

281 Human prostate cancer cell lines were used as models, as they

282 gen-dependent and androgen-independent human prostate cancer cell lines were used to test the effects

283 he effects of MM45 have been investigated in prostate cancer cell lines where it has been shown to in

284 rostatic intraepithelial neoplasia, and four prostate cancer cell lines, whereas B7-H1 is rarely expr

285 o augment endogenous KAI1 gene expression in prostate cancer cell lines, whereas silencing NDRG1 was

286 H was determined also in the metastatic PC-3 prostate cancer cell line, which exhibits increased expr

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

288 We also identified a panel of melanoma and prostate cancer cell lines whose ATF2 expression is inve

289 4-2B cell line, a variant of the LNCaP human prostate cancer cell line with propensity for bone metas

290 Treatment of prostate cancer cell lines with a C21-based peptide spec

291 treatment of androgen receptor (AR)-positive prostate cancer cell lines with androgens.

292 and orthotopic transplants of various human prostate cancer cell lines with AR over-expression or kn

293 clioquinol alone exhibits similar effects in prostate cancer cell lines with elevated copper at conce

294 RNA profiling of human prostate cancer cell lines with various degrees of AAV t

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

296 mediated proliferation of androgen-sensitive prostate cancer cell lines, with minimal toxicity in AR-

297 ecretomes of all of the androgen-independent prostate cancer cell lines, with no detectable secretion

298 ighly potent against a panel of melanoma and prostate cancer cell lines, with the best compound havin

299 ls of ANCCA are found in hormone-independent prostate cancer cell lines, xenograft tumor, and a subse

300 s 2 bp (TT) deletion, was found in two of 30 prostate cancer cell lines/xenografts and nine of 89 loc