ライフサイエンスコーパス: PC-3 cell

1 ng and cell proliferation in prostate cancer PC-3 cells.

2 WL-276 also effectively induced apoptosis in PC-3 cells.

3 ss fibers and microtubules in both DU145 and PC-3 cells.

4 ells (androgen receptor positive) but not in PC-3 cells.

5 creased when compared with that of wild-type PC-3 cells.

6 her lipids affect the release of exosomes in PC-3 cells.

7 ach metallated conjugate was evaluated using PC-3 cells.

8 cetaxel treatment, and inhibited invasion of PC-3 cells.

9 ced VEGF expression in human prostate cancer PC-3 cells.

10 oter activity in 12-lipoxygenase-transfected PC-3 cells.

11 nt analogue, having IC50 = 0.082 muM against PC-3 cells.

12 ted G(1) phase-specific cell cycle arrest in PC-3 cells.

13 e shown to interact with the F-5 fragment in PC-3 cells.

14 decrease of nuclear translocation of p65 in PC-3 cells.

15 rzb/sFRP3 decreased the invasive capacity of PC-3 cells.

16 locked Wnt-mediated osteoblastic activity in PC-3 cells.

17 ent in inhibiting cell-invasion/migration in PC-3 cells.

18 or formation when conditionally expressed by PC-3 cells.

19 optosis in LNCaP cells, but not in DU-145 or PC-3 cells.

20 viously raised against human prostate cancer PC-3 cells.

21 enesulfonamide hydrochloride (W-7) than were PC-3 cells.

22 tion in a dose-dependent manner in LNCaP and PC-3 cells.

23 specifically internalized in GRPR-expressing PC-3 cells.

24 rogen-independent (AI) LNCaP C-81 as well as PC-3 cells.

25 y target GRPrs on human, prostate, cancerous PC-3 cells.

26 es were not produced in androgen-independent PC-3 cells.

27 -rP1, but not in mac25/IGFBP-rP1-transfected PC-3 cells.

28 ependent manner in prostate cancer LNCaP and PC-3 cells.

29 cells underwent apoptosis more rapidly than PC-3 cells.

30 ft in Bcl-2/Bax levels favoring apoptosis in PC-3 cells.

31 lation of the Retinoblastoma (Rb) protein in PC-3 cells.

32 activity toward PSMA-negative cells, such as PC-3 cells.

33 ecreased in AS C-33 cells but not AI C-81 or PC-3 cells.

34 leotide restored sensitivity to apoptosis in PC-3 cells.

35 -responsive LNCaP and androgen-nonresponsive PC-3 cells.

36 olytic activity toward PSMA cDNA-transfected PC-3 cells.

37 using resistance to STS-induced apoptosis in PC-3 cells.

38 nd Bcl-X(L) was found to be overexpressed in PC-3 cells.

39 protein alone, induced apoptosis in >80% of PC-3 cells.

40 (ADP-ribose) polymerase, in LNCaP but not in PC-3 cells.

41 ulation of NF-kappaB observed in I3C treated PC-3 cells.

42 OPN potentiated the DUN-induced apoptosis of PC-3 cells.

43 rostate cancer and metastasis tissues and in PC-3 cells.

44 he activation of alpha(v)beta(3)-integrin on PC-3 cells.

45 d augmented the LCoR-dependent repression in PC-3 cells.

46 nd demonstrated similar internalization into PC-3 cells.

47 1 promoter activity and P-Rex1 expression in PC-3 cells.

48 -positive LNCaP cells but not in AR-negative PC-3 cells.

49 poptotic cell death in human prostate cancer PC-3 cells.

50 tive role of Red-Br-nos-induced autophagy in PC-3 cells.

51 lso suppressed the growth of prostate cancer PC-3 cells.

52 d successfully to A549 as well as DU 145 and PC-3 cells.

53 ectin-binding determinants on FT-upregulated PC-3 cells.

54 hat LOX-PP has other mechanisms of action in PC-3 cells.

55 GI 50 = 40 nM was the most potent versus the PC-3 cells.

56 soforms in invasive prostate adenocarcinoma (PC-3) cells.

57 d IL-8 at levels similar to that secreted by PC-3 cells (100-170 ng/10(6) cells) were characterized.

58 3, FT6, or FT7 expression induced robust PCa PC-3 cell adhesion to bone marrow (BM) endothelium and t

59 SDF-1alpha increased PC-3 cell adhesion to the human umbilical vein endotheli

60 ses, we undertook gene expression studies in PC-3 cells after cotreatment of 1alpha,25(OH)2D3 plus TS

61 In PC-3 cells, Akt deactivation does not lead to cytochrome

62 The Rho-0 variants of LNCaP and PC-3 cells also resisted PEITC-mediated autophagy.

63 A xenograft model using PC-3 cells and Caenorhabditis elegans expressing a lgg-1

64 orescent protein into LNCaP, MDA-Pca-2b, and PC-3 cells and confirmed its specific mitochondrial loca

65 ards the anti-angiogenic isoform VEGF165b in PC-3 cells and decreased tumour growth when administered

66 s proved on analysis of the genomic DNA from PC-3 cells and DNA isolated from melanoma tissues.

67 Trypsinogen IV was cloned from PC-3 cells and expressed in CHO cells, where it was also

68 and sequenced the full-length TxS cDNA from PC-3 cells and found two changes in the amino acid resid

69 ted with individual LPA(1)(-3) receptors, in PC-3 cells and in human platelets that endogenously expr

70 In both stably and transiently transfected PC-3 cells and in LNCaP cells, NKX3.1 expression increas

71 hPXR, led to nuclear translocation of PXR in PC-3 cells and increased expression of cytochrome P450 3

72 ase activity was found in 12-LOX-transfected PC-3 cells and inhibition of PI 3-kinase by LY294002 sig

73 nt/beta-catenin signaling in prostate cancer PC-3 cells and inhibits PC-3 cell proliferation.

74 ve toxicity of WL-276 against drug-resistant PC-3 cells and its in vivo suppression of PC-3 prostate

75 contributors to IGFBP-3-induced apoptosis in PC-3 cells and may play a wider role in the antiprolifer

76 g mRNA encoding green fluorescent protein in PC-3 cells and siRNA directed against the neurotrophin r

77 Anchorage-independent growth of the PC-3 cells and tumor formation in mouse xenografts of bo

78 tors, and their main splice variant, SV1, in PC-3 cells and tumor xenografts was demonstrated by RT-P

79 specifically internalized at 37 degrees C in PC-3 cells and was stable in mouse plasma.

80 glioblastoma (U-373) and prostate carcinoma (PC-3) cells, and concurrently inhibited phosphorylation

81 These changes in the biology of PC-3 cells are associated with a decrease in the express

82 PC-3 cells are known to synthesize and respond to IGF-II

83 ion of p21(WAF) in a p53-independent manner (PC-3 cells are p53 null).

84 ly greater in the more metastatic DU-145 and PC-3 cells as compared with LNCaP cells.

85 (177)Lu-NeoBOMB1 radioligands was studied in PC-3 cells at 37 degrees C, and their metabolic stabilit

86 tion of (99m)Tc radioligands was compared in PC-3 cells at 37 degrees C.

87 Radioligands poorly internalized in PC-3 cells at 37 degrees C.

88 on of the Akt signaling pathway and enhanced PC-3 cell attachment.

89 NKX3.1 expression in PC-3 cells attenuated the ability of insulin-like growth

90 In PC-3 cells, BBS stimulation of GRP-R resulted in the up-

91 Ligand binding assay found that PC-3 cells binded to SQ29548, a high-affinity TP antagon

92 3 inhibited cell proliferation of DU-145 and PC-3 cells (both cells express GSTpi), but not of LNCaP

93 sed the CXCR4 mRNA and protein expression in PC-3 cells but not in LNCaP cells.

94 kappaB-dependent transcriptional activity in PC-3 cells but not in LNCaP cells.

95 ncer HCT-116 cells and human prostate cancer PC-3 cells, but not a normal prostate epithelial cell li

96 TNF activated Akt in PC-3 cells, but not in DU145 cells, and the ability of T

97 ogical inhibition of PI 3-kinase activity in PC-3 cells, but not in DU145 cells.

98 ession of green fluorescent protein (GFP) in PC-3 cells, but not in HeLa cells.

99 in activation of Bax in wild-type LNCaP and PC-3 cells, but not in their respective Rho-0 variants.

100 gene expression were elevated in DU-145 and PC-3 cells, but paradoxically, LNCaP cells had undetecta

101 Suppression of NF-kappaB activity in PC-3 cells by a mutant IkappaBalpha super-repressor aden

102 tered expression of Cdc25C in C-33 cells and PC-3 cells by cDNA and/or shRNA transfection is associat

103 Inhibition of aneuploidy in p53 null PC-3 cells by DN-HSF1 expression was recapitulated by ex

104 hat adaphostin inhibits the proliferation of PC-3 cells by inducing a G(1) phase cell cycle arrest.

105 spase-independent ROS-dependent apoptosis in PC-3 cells by Red-Br-nos, a member of the noscapinoid fa

106 ting RelB in aggressive androgen-independent PC-3 cells by stable or conditional expression of a domi

107 Treatment of PC-3 cells by U46619, a TP agonist, induced PC-3 cell co

108 rostate LNCaP, but not in androgen-resistant PC-3 cells, by the induction of cytochrome c release, ac

109 This lack of functional E-cadherin in PC-3 cells coincided with a markedly different morpholog

110 e was no difference in tumor growth in mac25 PC-3 cells compared to control.

111 OD levels were found to be lower in parental PC-3 cells compared to nonmalignant, immortalized human

112 fect of 4 and (R)-4 in alpha(1d)-AR silenced PC-3 cells confirmed that their anticancer activity was

113 Southern blot analyses indicate that PC-3 cells contain an amplified Rad9 copy number.

114 PC-3 cells by U46619, a TP agonist, induced PC-3 cell contraction, which was blocked by pretreatment

115 wer Rad9 protein levels in CWR22, DU145, and PC-3 cells correlated with reduction of tumorigenicity i

116 We found that in migrating PC-3 cells, CtsH was co-localized with talin in the foca

117 Finally, media collected from PC-3 cell cultures, after BBS treatment, stimulated an N

118 In fact, 6m-hIGFBP-3 stimulated PC-3 cell death and stimulated apoptosis-induced DNA fra

119 riazole-mediated inactivation of catalase in PC-3 cells demonstrated increases in intracellular stead

120 We established stable cell colonies of PC-3 cells, depleted of CXCR1, using lentiviral plasmids

121 -HSF1 dramatically alters the DNA content of PC-3 cells (derived from p53 null prostatic carcinoma) a

122 Ectopic expression of USF2 in PC-3 cells did not affect the cell proliferation rate of

123 Interestingly, PC-3 cells did not respond to FGF-2, consistent with pre

124 nal genes associated with tributyrin-induced PC-3 cell differentiation and to gain some insight into

125 patterns with those of MPA, which initiates PC-3 cell differentiation by a dissimilar mode of action

126 ndependent genes in the processes leading to PC-3 cell differentiation induced by tributyrin and MPA.

127 f a group of these genes, which included the PC-3 cell differentiation marker keratin 17, was confirm

128 y and strongly bound on the cell membrane of PC-3 cells displaying low internalization, as expected f

129 LNCaP cells in a dose-dependent manner, with PC-3 cells displaying the greatest sensitivity to Apo-2L

130 Second, enforced Bcl-2 expression in PC-3 cells does not confer protection against the induct

131 tion in HEK-GRPR cells and Ca(2+) release in PC-3 cells (EC(50) = 1.3 nM).

132 fficiencies and VEGF inhibition in LNCaP and PC-3 cells exhibited the following trend: transferrin-PL

133 PC-3 cells expressed 50 times more Dickkopf-1 (DKK1), an

134 Inhibition of aneuploidy in PC-3 cells expressing DN-HSF1 was associated with delaye

135 When cellular morphology was examined, PC-3 cells expressing Frzb/sFRP3 exhibited an increase i

136 ted that Fas-mediated apoptosis in H1299 and PC-3 cells expressing p53 mutant 143Ala occurred only wi

137 a distinct survival mechanism that protects PC-3 cells from apoptotic signals emanating from PI3K in

138 ession of constitutively active Akt protects PC-3 cells from celecoxib-induced apoptosis.

139 g adenoviral vectors significantly protected PC-3 cells from toxicity and oxidative stress induced by

140 formation of lamellipodia in both DU145 and PC-3 cells, further supporting the concept that Stat3 pr

141 The four compounds inhibited prostate cancer PC-3 cell growth in a dose-dependent manner, whereas CG

142 androgen-independent human prostate cancer (PC-3) cells' growth rate in vitro and in vivo.

143 ution showed that 50-60% of Ad-NudC-infected PC-3 cells have a G2/M-phase DNA content compared to abo

144 ound that LNCaP and DU-145 cells and not the PC-3 cells have HPG-1 expression, with LNCaP cells havin

145 C(50) 0.12-0.20 microM), and less so against PC-3 cells (IC(50) 8-13 microM).

146 tly, TEM4-18 cells were more aggressive than PC-3 cells in a murine metastatic colonization model.

147 n PC-3 cells inhibited the tumorigenicity of PC-3 cells in an in vivo nude mice xenograft model (80-9

148 cells were much less invasive than parental PC-3 cells in assays that involve matrix barriers.

149 ity effect against Caco-2, HepG-2, MCF-7 and PC-3 cells in comparison with other NPs and free protein

150 the invasion capability (80% inhibition) of PC-3 cells in matrix gel assay.

151 rprisingly, were less invasive than parental PC-3 cells in other contexts in vitro.

152 that p45-sErbB3 enhances the invasiveness of PC-3 cells in part by stimulating the secretion of osteo

153 ls in vitro and prevented the s.c. growth of PC-3 cells in severe combined immunodeficient (SCID) mic

154 ly decreased anchorage-independent growth of PC-3 cells in soft agar (90-98% inhibition) and the inva

155 Transient transfection of BRCC2 cDNA into PC-3 cells in the presence of a broad-range caspase inhi

156 64)Cu and evaluated for internalization into PC-3 cells in vitro and for in vivo tumor uptake in mice

157 ted many of the malignant characteristics of PC-3 cells in vitro and prevented the s.c. growth of PC-

158 JMR-132 suppressed the proliferation of PC-3 cells in vitro in a dose-dependent manner and signi

159 tion, migration and invasion capabilities of PC-3 cells in vitro.

160 ect of 23-kDa PRL on the growth of DU145 and PC-3 cells in vivo may result from the combined effects

161 NKX3.1 expression in PC-3 cells increased insulin-like growth factor binding

162 Ectopic PSMA expression on PC-3 cells increased the invasive capacity of cells in i

163 60 cell lines and more extensive testing in PC-3 cells indicated that the mean concentration for tot

164 n androgen receptor-negative prostate cancer PC-3 cells, indicating an androgen receptor-dependent ev

165 cyclin E expression in U937 cells but not in PC-3 cells, indicating underlying differences in the mec

166 ent transfection of PMP24 into LNCaP(CS) and PC-3 cells induced a significant reduction in cell growt

167 ediated knockdown of KLF6, LCoR, or CtBP1 in PC-3 cells induced expression of CDKN1A and CDH1 and add

168 lular level, expression of NudC in DU145 and PC-3 cells inhibited cell proliferation at 48 h after Ad

169 Importantly, expression of USF2 in PC-3 cells inhibited the tumorigenicity of PC-3 cells in

170 Expression of NudC in DU145 or PC-3 cells inhibited tumor growth in a subcutaneous xeno

171 n of known prostate cancer cells (LAPC-9 and PC-3 cells) into the tibia of SCID mice.

172 First, the Bcl-xL/BAD ratio in PC-3 cells is at least an order of magnitude greater tha

173 at SDF-1alpha-induced expression of CXCR4 in PC-3 cells is dependent on MEK/ERK signaling cascade and

174 contrast, the LPA-stimulated rho response in PC-3 cells is dependent on PDZrhoGEF expression.

175 the adaphostin-mediated cell cycle arrest of PC-3 cells is dependent upon activation of the p38 MAPK.

176 ction of apoptosis by celecoxib in LNCaP and PC-3 cells is independent of Bcl-2.

177 When applied to human prostate cancer PC-3 cells, it was able to inhibit the proliferation, an

178 iated knockdown of PIP5K1alpha in aggressive PC-3 cells leads to a reduced AKT activity and an inhibi

179 beled with (111)In and evaluated in vitro in PC-3 cell line and in vivo in PC-3 tumor-bearing nude mi

180 eatment with RAD001, with the PTEN-deficient PC-3 cell line showing the greater sensitivity.

181 (PPC-1) but did not bind to the NRP-negative PC-3 cell line, and binding was observed with liposomal

182 inactive Stat5 proteins were detected in the PC-3 cell line, which correlated with resistance to DNSt

183 otype and highly tumorigenic behavior of the PC-3 cell line.

184 xorubicin as compared with the PTEN-negative PC-3 cell line.

185 LNCaP and DU145 cell lines than it is in the PC-3 cell line.

186 ere more sensitive to WL-276 than the parent PC-3 cell line.

187 LNCaP(CS) and the androgen receptor-negative PC-3 cell line; both exhibited dense methylation in the

188 In addition, three PC-3 cell lines with acquired drug resistance against st

189 in the prostate carcinoma LNCaP, DU145, and PC-3 cell lines, HEK293 cells, the EBV-immortalized cell

190 MT in human prostate cancer LNCaP, C4-2B and PC-3 cell lines, while small interfering RNA knockdown o

191 oliferative potencies in both MDA-MB-231 and PC-3 cell lines.

192 he growth of human prostate cancer LNCaP and PC-3 cell lines.

193 ndogenous concentrations in prostate cancer (PC-3) cell lysate.

194 that a factor protecting the mitochondria of PC-3 cells mediates resistance to STS-induced apoptosis.

195 I-Tyr(4)]BBN were conducted in GRPR-positive PC-3 cell membranes.

196 against [(125)I-Tyr(4)]BBN in GRPR-positive PC-3 cell membranes.

197 ivity or blockade of TXA(2) function reduced PC-3 cell migration on fibronectin, while having minimal

198 The PEITC-mediated inhibition of PC-3 cell migration was statistically significantly atte

199 them unoccupied, whereas the more metastatic PC-3 cells occupied all available Tepuis.

200 opic expression of Bcl-xL, but not Bcl-2, in PC-3 cells offered significant protection against the ce

201 ncing significantly reduced the migration of PC-3 cells on fibronectin and invasion through Matrigel.

202 id not affect the cell proliferation rate of PC-3 cells on plastic surfaces.

203 oC is required for the invasive phenotype of PC-3 cells.Oncogene advance online publication, 28 Novem

204 Similar effects of DIM were observed in PC-3 cells only when these cells were co-transfected wit

205 0% in anti-CCL2-treated animals from VCaP or PC-3 cell osseous lesions) and microvessel density was d

206 tingly, prolonged downregulation of Hsp72 in PC-3 cells over 3 weeks aggravated these effects, as wel

207 PC-3 cells overexpressing AKR1C2 and, to a lesser extent

208 ion of the expression of MMP-9 in DU-145 and PC-3 cells produced concomitant inhibition of the gene e

209 PC-3 cell proliferation and (177)Lu-RM2 uptake after tre

210 nly regulates cell survival but also affects PC-3 cell proliferation by retarding G(1) to S transitio

211 g in prostate cancer PC-3 cells and inhibits PC-3 cell proliferation.

212 y NKX3.1 and abrogated NKX3.1 suppression of PC-3 cell proliferation.

213 In PC-3 cells, radiation upregulated TNF-alpha protein lead

214 its precursor hairpin RNA (pre-miR-373) into PC-3 cells readily induced E-cadherin expression.

215 luble VEGF receptor-3/Flt4 fusion protein by PC-3 cells reduced intratumoral lymphatics by 100% in s.

216 ular endothelial growth factor-C (VEGF-C) in PC-3 cells reduced intratumoral lymphatics by 99% in s.c

217 ype AR-mediated transactivation in LNCaP and PC-3 cells, respectively.

218 Overexpression of 12-lipoxygenase in PC-3 cells resulted in a 3-fold increase in VEGF protein

219 ons of p300 in the presence of bombesin into PC-3 cells resulted in a linear increase in AR transacti

220 We showed that expression of Frzb/sFRP3 in PC-3 cells resulted in decreased colony formation in sof

221 Expression of these proteins in PC-3 cells resulted in intracellular accumulation.

222 12 neuronal-like cells or 50B11 neurons with PC-3 cells resulted in neurite outgrowth in neuronal cel

223 adherin promoter, and inhibition of Kaiso in PC-3 cells results in increased E-cadherin expression, a

224 oprecipitation (ChIP) assays of the HS27 and PC-3 cells revealed the binding of Sp1 protein to PTTG p

225 ogenous P-Rex1 in metastatic prostate cancer PC-3 cells selectively inhibited Rac activity and reduce

226 d potent cytotoxicity against both LNCaP and PC-3 cells, seven only against LNCaP, and one solely aga

227 PC-3 cells showed increased expression of MMP-9 and memb

228 increased cytotoxicity toward drug-resistant PC-3 cells shows the clinical potential of WL-276 agains

229 cell surface derived endocytic vesicles, in PC-3 cells, suggesting impaired trafficking to the cell

230 re much weaker in metastatic prostate cancer PC-3 cells than in non-metastatic prostate cancer cells,

231 the minor HMGA1a fraction isolated from the PC-3 cells that were not treated with butyrate.

232 mediated osteoblastic activity in osteolytic PC-3 cells, the cells were stably transfected with DKK-1

233 Celecoxib and DMC block Akt activation in PC-3 cells through the inhibition of phosphoinositide-de

234 Exposure of PC-3 cells to 10 microM PEITC also resulted in a time-de

235 Expression of PTEN in PC-3 cells to a level comparable with that endogenously

236 Exposure of PC-3 cells to an apoptosis-inducing concentration of PEI

237 ficantly attenuated the metastatic spread of PC-3 cells to bone.

238 Exposure of PC-3 cells to growth-suppressive concentrations of SFN r

239 ignificantly increased following exposure of PC-3 cells to hypoxia.

240 Decreasing DKK-1 enabled PC-3 cells to induce osteoblastic activity, including al

241 enase inhibitors induce androgen-independent PC-3 cells to mature into cells with a phenotype that re

242 We engineered LNCaP and PC-3 cells to overexpress Bcl-xL protein and demonstrate

243 Exposure of LNCaP and PC-3 cells to pharmacologic concentrations of PEITC resu

244 d the ability of 12-lipoxygenase-transfected PC-3 cells to stimulate endothelial cell migration, sugg

245 SR12813 pretreatment increased resistance of PC-3 cells to Taxol and vinblastine, as assessed by viab

246 tisense down-regulation of Bcl-xL sensitizes PC-3 cells to the apoptotic effect of LY294002.

247 Exposure of PC-3 cells to these agents led to Akt dephosphorylation

248 in levels in curcumin plus radiation-treated PC-3 cells, together, altered the Bcl2 : Bax ratio and t

249 urthermore, elevated FT7 expression promoted PC-3 cell trafficking to and retention in BM through an

250 evealed an elevated VEGF transcript level in PC-3 cells transfected with a 12-lipoxygenase expression

251 ondria of LNCaP cells, MDA-PCa-2b cells, and PC-3 cells transfected with a TARP-expressing plasmid.

252 tivity was also evaluated in LNCaP cells and PC-3 cells transfected with wild-type androgen receptor.

253 of G1 cell cycle arrest was also observed in PC-3 cells treated with I3C, which may be due to the obs

254 In PC-3 cells treatment repressed the expression of anti-ap

255 aminoglycoside antibiotic neomycin inhibited PC-3 cell tumor growth in athymic mice and was accompani

256 ctions of the Bax overexpression system into PC-3 cell tumors in nude mice in vivo caused a 25% regre

257 man prostate cancer cell lines LNCaP but not PC-3 cells undergo apoptosis after treatment with the pr

258 verexpression of p65 subunit of NF-kappaB in PC-3 cells up-regulated CXCR4 receptor expression and in

259 Subsequently, we knocked down SMRT levels in PC-3 cells using a small interfering RNA (siRNA) approac

260 The DATS-induced cell cycle arrest in PC-3 cells was associated with increased Tyr(15) phospho

261 DATS-induced apoptosis in PC-3 cells was associated with phosphorylation of Bcl-2,

262 Apo-2L/TRAIL-induced apoptosis of PC-3 cells was associated with the processing of caspase

263 The biosynthesis of TXA(2) in PC-3 cells was dependent on COX-2, and to a lesser exten

264 TxS expressed in PC-3 cells was enzymatically active and susceptible to c

265 CaSR signaling in PC-3 cells was evaluated by measuring the elevated [Ca2+

266 Phosphorylation of Bcl-2 in DATS-treated PC-3 cells was fully blocked in the presence of JNK-spec

267 Indeed, AR transactivation in PC-3 cells was preferentially inhibited at the low conce

268 By transfecting p53 in PC-3 cells, we demonstrate that low concentrations of p5

269 Using PC-3 cells, we obtained similar displacement curves and

270 By inhibiting the expression of ADAM15 in PC-3 cells, we showed decreased cell migration and adhes

271 pathways were upregulated very rapidly when PC-3 cells were exposed to selenium.

272 h orthotopic and intratibial tumor growth of PC-3 cells were more potently inhibited by dual SFK and

273 The Rho-0 variants of LNCaP and PC-3 cells were more resistant to PEITC-mediated ROS gen

274 ded with a markedly different morphology and PC-3 cells were not found to form close cell-cell associ

275 LnCap and DU145 cells were very sensitive, PC-3 cells were relatively resistant, and DuPro cells we

276 Bcl-2 overexpressing PC-3 cells were significantly more resistant to apoptosi

277 e of MnSOD in the prostate cancer phenotype, PC-3 cells were stably transfected with MnSOD cDNA plasm

278 that the levels of Sp1 protein are higher in PC-3 cells when compared to levels in HS27 cells, possib

279 nt osteonectin increased the invasiveness of PC-3 cells, whereas osteonectin-neutralizing antibodies

280 ic acid (MPA), induce the differentiation of PC-3 cells, which are derived from a human androgen-inde

281 factor YB-1 and its targets HER2 and EGFR in PC-3 cells, which could be rescued by the stable express

282 However, in H358 and PC-3 cells, which express a serine phosphorylated topois

283 cer cells showed that PCPH overexpression in PC-3 cells, which express nearly undetectable PCPH level

284 ha-stimulated degradation of IkappaBalpha in PC-3 cells, which was associated with the inhibition of

285 Treatment of PC-3 cells with a COX-1 selective inhibitor, piroxicam,

286 Treatment of DU-145 and PC-3 cells with a selective chemical inhibitor of MMP-9

287 Transient transfection of LNCaP and PC-3 cells with Atg5-specific small interfering RNA conf

288 Transient transfection of PC-3 cells with Chk2-specific small interfering RNA dupl

289 chanistic studies showed that stimulation of PC-3 cells with extracellular Ca(2+) resulted in an incr

290 Treatment of LNCaP and PC-3 cells with hCG modestly reduced cell viability with

291 nt on reduction of AKT activity in LNCaP and PC-3 cells with high constitutive AKT activity, but not

292 Consistent with these results, treatment of PC-3 cells with PEITC resulted in translocation of p66(S

293 Treatment of PC-3 cells with SDF-1alpha leads to nuclear translocatio

294 ogenic splice isoform, VEGF165b, was seen in PC-3 cells with SRPK1 knockdown (KD).

295 Pretreatment of PC-3 cells with the mTOR inhibitor, rapamycin, inhibited

296 Treatment of PC-3 cells with troglitazone or Delta2-TG led to reduced

297 ivated by TP activation, and pretreatment of PC-3 cells with Y27632, a Rho kinase (ROCK) inhibitor, b

298 (99m)Tc-SARNCs specifically internalized in PC-3 cells, with (99m)Tc-SARNC5 displaying the fastest i

299 under hypoxic growth conditions in HT-29 and PC-3 cells, with upregulation of the SKIP3 mRNA transcri

300 nding assay using (125)I-[Tyr(4)]BBN against PC-3 cells yielded a 50% inhibitory concentration value