ライフサイエンスコーパス: PC3 cell

1 tion and metastasis seen in mock-transfected PC3 cells.

2 is critical for anticancer activity against PC3 cells.

3 nscript A-to-I editing detected in DU145 and PC3 cells.

4 gests that more than one step is affected in PC3 cells.

5 y different RNA editing enzymes in DU145 and PC3 cells.

6 viral replication cycle that is inhibited in PC3 cells.

7 e cancer LNCaP and its derivative C4-2B, and PC3 cells.

8 yxin formed a complex with ezrin in MCF7 and PC3 cells.

9 uction in LNCaP cells but only low levels in PC3 cells.

10 ls as compared with control mock-transfected PC3 cells.

11 pression was much lower than that of control PC3 cells.

12 to selenite-induced apoptosis than p53-null PC3 cells.

13 as maspin siRNA decreased CK18 expression in PC3 cells.

14 protein in RWPE-1 and DU145 cells but not in PC3 cells.

15 ibitory effects on migration and invasion of PC3 cells.

16 6) leads to microtubule depolymerization in PC3 cells.

17 l cancer KYSE 150 cells, and prostate cancer PC3 cells.

18 eactivity to other family members in HeLa or PC3 cells.

19 sensitivity to UV than observed in wild-type PC3 cells.

20 lowing UV treatment and shown to increase in PC3 cells.

21 d-p53 in both control and bcl-2-transfectant PC3 cells.

22 nce was observed in 22Rv1, DU145, LNCaP, and PC3 cells.

23 the down-regulation of Cdc6 transcription in PC3 cells.

24 drogen-independent metastatic human prostate PC3 cells.

25 te cancer cells, including DU145, LNCaP, and PC3 cells.

26 ecules are detected, especially in DU145 and PC3 cells.

27 issue-specific colonization of human bone by PC3 cells.

28 served in the tumors from 12-LOX-transfected PC3 cells.

29 DA-MB-231 cells in comparison to AR-negative PC3 cells.

30 l-mesenchymal transition and invasiveness in PC3 cells.

31 an localize to the nucleus in both DU145 and PC3 cells.

32 as the serine peptidases CTSA and SCPEP1, in PC3 cells.

33 1,25D(3)-induced CYP24A1 mRNA expression in PC3 cells.

34 ndogenous CYP24A1 mRNA level in TBBz-treated PC3 cells.

35 , colon cancer HCT116 and prostate carcinoma PC3 cells.

36 an increased uptake of W106F-cystatin C, in PC3 cells.

37 caspase-9 but not caspase-3 was activated in PC3 cells.

38 ation to the protein expression in LnCAP and PC3 cells.

39 d to be potential target genes of miR-182 in PC3 cells.

40 duce integrin activity and cell migration in PC3 cells.

41 SubA has no effect on Hep3B and PC3 cells.

42 orthotopic implantation of DsRed-expressing PC3 cells.

43 ormation of peripheral adhesion complexes in PC3 cells.

44 ve in suppressing the growth and motility of PC3 cells.

45 ctin- and dynamin-dependent pathway to enter PC3 cells.

46 sed glycerophosphocholine and tCho levels in PC3 cells.

47 is markedly reduced when Pin1 is depleted in PC3 cells.

48 effect on proliferation of prostate cancer (PC3) cells.

49 androgen receptor-negative prostate cancer (PC3) cells.

50 In PC3 cells, 13-(S)-HODE, a 15-LOX-1 metabolite, up-regula

51 Pancreatic cancer B x PC3 cells (3 x 10(7)) were injected into the tail of pan

52 CAP cells as well as in androgen-independent PC3 cells abrogates DHT- and/or EGF-induced Erk signalin

53 ere solely arrested in mitosis on treatment, PC3 cells accumulated in G2 phase and mitosis, suggestin

54 PC3 cells adhered to and migrated on vitronectin (VN), a

55 rm RR holoenzyme and maintain RR activity in PC3 cells after UV treatment.

56 Thus, in PC3 cells, alpha(v)beta(3) mediates cell migration and P

57 ase-negative OPAL codon mutant, in DU145 and PC3 cells also increased cell death.

58 PC3 cells also showed a strong decrease in phosphorylate

59 al PI3K activity was mediated by p110beta in PC3 cells and by both p110beta and p110delta in LNCaP ce

60 osis in androgen-independent prostate cancer PC3 cells and compared its effect with that of staurospo

61 aluate ROK activity in human prostate cancer PC3 cells and endothelial cells (HUVECs).

62 the myosin phosphatase was phosphorylated in PC3 cells and HUVECs, and phosphorylation of MYPT1 and t

63 ogenous ceramide overcomes the lesion in the PC3 cells and induces apoptosis.

64 ntrast, hRRM2 was up-regulated by UV in both PC3 cells and KB cells.

65 unx2 and Fra-2 are higher in the OC-positive PC3 cells and osteoblasts, compared with the OC-negative

66 and gelatinolytic activity as compared with PC3 cells and PC3 cells expressing mutant OPN in integri

67 ntrol cancer cells of AGS cells, VERO Cells, PC3 cells and SKOV-3 cells.

68 er, the increased cell proliferation rate of PC3 cells and TREK-1 overexpressing CHO cells could be r

69 sie Blue-stained band) was down-regulated in PC3 cells and up-regulated in KB cells after UV exposure

70 a tissues, 15-LOX-2 mRNA was not detected in PC3 cells, and they did not produce detectable 15-HETE f

71 ibody to alpha(v)beta(5) (and in the case of PC3 cells, anti-alpha(v)beta(3)) resulted in significant

72 ycle arrest with decline in CDK1 activity in PC3 cells, apoptosis of SUDHL4 cells occurred without ev

73 These results suggest that PC3 cells are deficient in both transcription of p53R2 a

74 Human prostate cancer PC3 cells are deficient in tensin relative to fibroblast

75 PC3 cells are dependent on PI-3K for survival and underg

76 ible to camptothecin-induced cell death, and PC3 cells are resistant.

77 Specifically, we demonstrated that PC3 cells are unable to elevate ceramide in response to

78 We selected PC3 cells as a test model system because of their highly

79 and longer doubling time of MBP-1 knockdown PC3 cells as compared with control mock-transfected PC3

80 own of PIP5K1alpha exerts similar effects on PC3 cells as ISA-2011B treatment, significantly inhibiti

81 Moreover, silencing of Hic-5 in PC3 cells as well as in the WPMY-1 human prostate stroma

82 only bcl-2 is down-regulated in both T24 and PC3 cells at 50 nM oligonucleotide concentration.

83 o trap and concentrate human prostate cancer PC3 cells at a predetermined site.

84 jugates selectively adhered to LNCaP but not PC3 cells at static and low shear (<1 dyn/cm2) but not h

85 Src mediates cell proliferation in DU145 and PC3 cells at the G1 phase of cell cycle.

86 DU145 and PC3 cells become sensitive to the negative effects of S1

87 in vitro, and in vivo shRunx2 expression in PC3 cells blocked their ability to survive in the bone m

88 Im inhibited the cell viability of DU145 and PC3 cells but did not affect the viability of fibroblast

89 that the p53R2 binding to hRRM1 decreased in PC3 cells but increased in KB cells after UV treatment.

90 Parthenolide causes oxidative stress in PC3 cells but not in PrEC cells, as determined by the ox

91 radiosensitization effect on prostate cancer PC3 cells but not on normal prostate epithelial PrEC cel

92 R-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells.

93 oss of viability of the human tumor HeLa and PC3 cells, but the coadministration of copper increases

94 nsible for the high hOC promoter activity in PC3 cells by binding to the OSE2, AP-1/VDRE, and OSE1 el

95 c expression of c-FLIP(L) in TRAIL-sensitive PC3 cells changed their phenotype from TRAIL sensitive t

96 n the Cdc6 promoter was substantially low in PC3 cells compared with BPH cells.

97 ferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells.

98 sed proteomic analysis on BRF1-overexpresing PC3 cells confirmed reduced levels of CFD in the secreto

99 sion showed that in contrast to LNCaP cells, PC3 cells constitutively expressed numerous antiviral ge

100 Experiments with latrunculin-A-treated PC3 cells corroborated these observations.

101 BrdU incorporation in PC3 cells could, however, be increased by overexpressing

102 r shown to exhibit increased cytotoxicity in PC3 cell culture medium that was already below pH 7.0 at

103 rBbKIm caused an arrest of the PC3 cell cycle at the G0/G1 and G2/M phases but did not

104 Runx2 siRNA treatment of PC3 cells decreased cell migration and invasion through

105 SR or TRPC6 expression in calcium-stimulated PC3 cells decreased cell proliferation and SOCE.

106 Transfection of PTEN into the PC3 cells decreased the activation of Akt and the downst

107 erin-11 in cadherin-11-expressing metastatic PC3 cells decreases cell motility and invasiveness.

108 cating that metastatic human prostate cancer PC3 cells deficient in DAB2IP (shDAB2IP) exhibit increas

109 In vitro, 12-LOX-transfected PC3 cells demonstrated a proliferation rate similar to n

110 Ribozyme suppression of MMP-9 expression in PC3 cells did not affect pro-MMP-9 activation or net MMP

111 Interestingly, PC3 cells do not express alpha-catenin, an actin binding

112 These effects were inhibited in PC3 cells engineered to express bcl2 (PC3-bcl2).

113 G(2)/M phase (89%); 2) induces cell death in PC3 cells even after the removal of the compound; 3) bin

114 d with the control clones, HOXB13-expressing PC3 cells exhibited significant inhibition of in vitro a

115 Moreover AIF-deficient PC3 cells exhibited substantial reduction of tumorigenic

116 was downregulated and p21 was upregulated in PC3 cells exposed to ATO.

117 the human prolactin receptor, but DU145 and PC3 cells express only low amounts of this receptor unti

118 While PC3 cells expressed higher levels of endogenous BRK than

119 inoculation into the prostate of nude mice, PC3 cells expressing core3 O-glycans produced much small

120 Xenografted PC3 cells expressing GPx3 showed reduction in tumor volu

121 ctivated cell sorter analysis suggested that PC3 cells expressing MBP-1-specific small interfering RN

122 ytic activity as compared with PC3 cells and PC3 cells expressing mutant OPN in integrin-binding doma

123 IL-1beta was significantly down-regulated in PC3 cells expressing TARP.

124 cancer cell line (PC3) that lacks Stat3 and PC3 cells expressing wild-type Stat3 or a Stat3 mutant c

125 Ectopic expression of p53 in PC3 cells for 44 hours did not reduce XIAP abundance or

126 n into athymic nude mice, 12-LOX-transfected PC3 cells formed larger tumors than did the controls.

127 indicate that CCL2 protects prostate cancer PC3 cells from autophagic death via the phosphatidylinos

128 onstrates that CCL2 protects prostate cancer PC3 cells from autophagic death, allowing prolonged surv

129 ecific knockdown of ALCAM in bone-metastatic PC3 cells greatly diminished both skeletal dissemination

130 rence with B1I combined with (223)Ra reduced PC3 cell growth in bone and significantly improved overa

131 ce with beta1I combined with (223)Ra reduced PC3 cell growth in bone and significantly improved overa

132 erestingly, AR gene transcripts in DU145 and PC3 cells harbored a large number of single base pair nu

133 ve clinical disease; (2) ERK5-overexpressing PC3 cells have enhanced proliferative, migrative and inv

134 In PC3 cells, however, these values are 10, 1, and 0.

135 In PC3 cells, hydroxyurea inhibited hRRM2 and resulted in i

136 NO66-overexpressing PC3 cells implanted into the femoral bone of male SCID m

137 ced apoptosis and inhibited proliferation of PC3 cells in culture, but both MDM2 overexpression and k

138 nant LOX-PP (rLOX-PP) inhibits the growth of PC3 cells in vitro by mechanisms that were not character

139 d the invasive phenotype in SPDEF expressing PC3 cells in vitro, suggesting that the effects of SPDEF

140 , restoration of wild-type p53 expression in PC3 cells increased cellular sensitivity to selenite and

141 terfering RNA (siRNA) silencing of maspin in PC3 cells increased HDAC activity.

142 EphA2 phosphorylation and cells rounding in PC3 cells, indicating EphA2-antagonizing activity of EM2

143 small interfering RNA kills prostate cancer PC3 cells, indicating that the TGFbeta2-NF-kappaB pathwa

144 Coculturing RhoA knockout fibroblasts and PC3 cells induced expression of proinflammatory genes in

145 In PC3 cells, inhibition of miR-1296 upregulated both MCM2

146 Invadopodia enable polarized invasion of PC3 cells into the gelatin matrix in a time-dependent ma

147 Depletion of INO80 in prostate cancer PC3 cells leads to increased R-loops.

148 alectin-3 knockdown in human prostate cancer PC3 cells led to cell-cycle arrest at G(1) phase, up-reg

149 Expression of antisense hRRM2 in PC3 cells led to decreased hRRM2 expression and resulted

150 cluding c-myc were overexpressed in both the PC3 cell line and DU145, but the PC3 to DU145 expression

151 (GI(50)) in the low micromolar range in the PC3 cell line and were thus selected for extensive furth

152 transfection of a full-length cDNA into the PC3 cell line confers NAAG-hydrolyzing activity that is

153 In addition, loss of RalA in the metastatic PC3 cell line inhibited bone metastasis but did not affe

154 pase cleavage in the prostate cancer-derived PC3 cell line is metabolically unstable in cells because

155 ppression of PS1 expression in p53-deficient PC3 cell line suggesting that inhibition of basal JNK ac

156 the function of TARP, we generated a stable PC3 cell line that expresses TARP in a constitutive mann

157 LNCaP cell line and the androgen-insensitive PC3 cell line to treatment with the topoisomerase I inhi

158 The highly invasive human prostate cancer PC3 cell line was found to express the alpha(v)beta3 int

159 TG003 decisively inhibited the growth of a PC3 cell line xenograft in nude mice.

160 We demonstrate that in the aggressive PC3 cell line, adhesion to fibronectin via beta1 integri

161 In the PC3 cell line, deletions are observed only when the d(TC

162 is down-regulated in the highly tumorigenic PC3 cell line, which suggests that, in addition to its f

163 t 10q23.1 (50-350 kb spanning SFTPA2) in the PC3 cell line.

164 nslocation are suppressed by thapsigargin in PC3 cell line.

165 ated enhanced cytotoxicity against 4T1.2 and PC3 cell lines compared to DOX and DOX-loaded POEG-b-PCC

166 is of gene expression from treated DU145 and PC3 cell lines demonstrate a close similarity of nelfina

167 ess conditions, AIF depletion from DU145 and PC3 cell lines led to significant reductions in cell sur

168 trated the highest activity against HePG and PC3 cell lines, with an IC(50) range of 11-17 uM.

169 t (DU145 and JCA1) and sensitive (ALVA31 and PC3) cell lines.

170 In PC3 cells, MDM2 inhibition resulted in elevated p21, Bax

171 We found that PC3 cells migrated more efficiently as multi-cellular cl

172 ortmannin, a PI 3-kinase inhibitor, prevents PC3 cell migration on both osteopontin and vitronectin;

173 3Ky significantly suppresses prostate cancer PC3 cell migration, invasion, and metastasis.

174 of Pak1, and not Pak6, resulted in impaired PC3 cell migration, the effects of Pak1 knockdown on tra

175 hat such activation was required for maximal PC3 cell mitogenesis, as measured by 5-bromo-2'-deoxy-ur

176 ly showed jumps in their force curves, while PC3 cells on bovine-serum-albumin- and antibody-treated

177 Untreated PC3 cells on Col-I or SCP1 cells, which express Col-I, p

178 n of platelet-type 12-LOX in prostate cancer PC3 cells or epithelial cancer A431 cells significantly

179 tly, holoclones derived from either cultured PC3 cells or holoclone-initiated tumors can be serially

180 demonstrated that restoring AR in epithelial PC3 cells or knockdown of AR in stromal WPMY1 cells supp

181 mutant forms of EGFR (Tyr(845)) or Stat5b in PC3 cells, or treatment with selective, catalytic inhibi

182 SE1, OSE2, and AP-1/VDRE, was established in PC3 cells (OSE1 > AP-1/VDRE > OSE2).

183 We show that DU145 and PC3 cells overexpress EGFR and migrate in a ligand (EGF)

184 PC3 cells overexpressing GPx3 reduced invasiveness in Ma

185 Moreover, PC3 cells overexpressing osteopontin (OPN) displayed an

186 [35S]methionine pulse experiments in PC3 cells overexpressing PTEN demonstrated that these ce

187 r resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulatio

188 significantly elevated p21 protein levels in PC3 cells (p53 null).

189 s study, we found that PDGF-D-overexpressing PC3 cells (PC3 cells stably transfected with PDGF-D cDNA

190 B1 expression was observed in MBP-1-depleted PC3 cells (PC3-4.2) upon serum stimulation, although the

191 Restoring AR in PC3 cells (PC3-AR9) results in decreased invasion in bon

192 To address PC3 cells' predominant Col-I binding molecules, an antib

193 Conversely, the overexpression of CLK1 in PC3 cells prevented TG003 from reducing cell proliferati

194 ein was no longer effective in up-regulating PC3 cell proliferation, invasion, and MMP-9 activation,

195 1) phase cell cycle arrest and inhibition of PC3 cell proliferation.

196 dentified in co-culture studies showing that PC3 cells promote osteoclastogenesis and inhibit osteobl

197 However, p53-expressing PC3 cells readily apoptosed when exposed to CKIs or when

198 ablation of PI4KIIIalpha in CXCR4-expressing PC3 cells reduced cellular invasion in response to a var

199 Ectopic expression of PSMA in PC3 cells reduced the invasiveness of these cells, sugge

200 , penetration was delayed by 10 to 30 min in PC3 cells relative to LNCaP cells.

201 ary transcription was delayed by 6 to 8 h in PC3 cells relative to LNCaP cells.

202 ADAR1 and ADARB1 were observed in DU145 and PC3 cells relative to the androgen-responsive LNCaP and

203 utamide via a cleavable linear tether enters PC3 cells, resides in cytosol, binds to the AR if presen

204 MDA-MB-435 and PC3 cells, resistant to DF 203, did not show drug-induce

205 blot analysis revealed that PFE treatment of PC3 cells resulted in (i) induction of Bax and Bak (proa

206 atment to human PCa LNCaP, C4-2, 22Rnu1, and PC3 cells resulted in a dose-dependent inhibition of cel

207 t of highly aggressive human prostate cancer PC3 cells resulted in a dose-dependent inhibition of cel

208 data demonstrated that uPA-uPAR knockdown in PC3 cells resulted in a dramatic reduction of tumor cell

209 Expression of TARP in PC3 cells resulted in a more rapid growth rate with a 5-

210 weekly) to athymic nude mice implanted with PC3 cells resulted in a significant inhibition of tumor

211 The induced expression of GPx3 in DU145 and PC3 cells resulted in an increase in reactive oxygen spe

212 h its role in invasion, depletion of CD97 in PC3 cells resulted in decreased bone metastasis without

213 of JunD expression using siRNA in DU145 and PC3 cells resulted in significant reduction in cell prol

214 Ectopic expression of TMEFF2 in DU145 and PC3 cells resulted in their prominent inhibition of grow

215 ansfection of ERK5wt and MEK5D constructs in PC3 cells results in predominant ERK5 nuclear localizati

216 Interestingly, ephrin-A1-induced PC3 cell retraction also requires LPA, which stimulates

217 Knockdown of GNA13 in highly invasive PC3 cells revealed that these cells depend on GNA13 expr

218 -catenin was re-introduced, the phenotype of PC3 cells reverted back to a more epithelial phenotype w

219 thraquinone fluorescence of targeted drug in PC3 cells showed initial cytosolic localization, indepen

220 n bovine-serum-albumin- and antibody-treated PC3 cells showed long membrane tethers.

221 d PC3-TR (a TRAIL-resistant subpopulation of PC3) cells showed increased c-FLIP(L) mRNA levels and ma

222 ble upregulation of TSPAN1 in both DU145 and PC3 cells significantly increased cell migration and ind

223 ic expression of miR-182 and miR-141/200a in PC3 cells significantly reduced protein levels, GNA13-3'

224 and silibinin in human prostate cancer (PCA) PC3 cells; silymarin is comprised of silibinin and its o

225 PC3 cells stably expressing CSR1 had an average threefol

226 lular delivery was tested in GRPR expressing PC3 cells stably transfected with a luciferase gene inte

227 found that PDGF-D-overexpressing PC3 cells (PC3 cells stably transfected with PDGF-D cDNA and referr

228 roscopy, which showed a higher percentage of PC3 cells staining positive for P-S319-Runx2 relative to

229 In PC3 cells, Stattic alone inhibited gene expression of CC

230 After i.v. injection, circulating PC3 cells successfully colonized implanted human bone fr

231 PUMA in response to 3beta-Adiol in LNCaP and PC3 cells, suggesting that FOXO3a mediates the apoptotic

232 as EGF-induced cyclin D1 mRNA expression in PC3 cells, suggesting that paxillin may regulate prostat

233 topographical change and ROS release at the PC3 cell surfaces.

234 rved higher degrees of ROS generation in the PC3 cells than DU145 and LNCaP, and that ROS generation

235 r transfection efficiency in HEK293, 3T3 and PC3 cells than with weight ratios of 3:7 or 7:3.

236 rovirus (hERV) envelope RNAs were present in PC3 cells that bind and activate OAS.

237 Highly invasive prostate cancer PC3 cells that constitutively express alpha(v)beta(3) ad

238 HUH7, A-172, and PC3 cells that expressed MAN2A1-FER were about 2-fold mo

239 which harbor the TMPRSS2-ERG gene fusion and PC3 cells that stably express a similar construct (fusio

240 vation of MAPK and PI3K activity in MCF7 and PC3 cells through its ability to form a complex with ezr

241 in the process of migration and invasion of PC3 cells through regulating processes essential for the

242 st that mevastatin inhibits cdk2 activity in PC3 cells through the inhibition of Thr-160 phosphorylat

243 Like DHA, the DHA metabolites a) induce PC3 cells to activate a peroxisome proliferator-activate

244 gnificantly reduced the ability of DU145 and PC3 cells to form large colonies in soft agar.

245 potently sensitizes radioresistant LNCaP and PC3 cells to gamma radiation, regardless of the status o

246 14-E,Z,Z,Z-eicosatetraenoate (5-HETE) causes PC3 cells to grow by an unknown mechanism.

247 A 72-h exposure of the MDA468 and PC3 cells to perifosine alone resulted in cell death in

248 LOX-PP was shown to sensitize both DU145 and PC3 cells to radiation-induced cell death determined in

249 we analyzed docetaxel-treated and nontreated PC3 cells to reveal proteome changes at the single-cell

250 loped with FAP-positive U87 and FAP-negative PC3 cells to test pharmacokinetics and binding specifici

251 kinase function reduced matrigel invasion of PC3 cells to the same extent as CD82 expression.

252 tion of JNK is required for sensitization of PC3 cells to TRAIL-induced apoptosis by translation inhi

253 PC3 cells transfected with 12-LOX displayed increased al

254 boxypeptidase were expressed in membranes of PC3 cells transfected with either pig folylpoly-gamma-ca

255 -induced gene activation was also present in PC3 cells transfected with the AR but not in the parenta

256 also present in prostate cancer CWR22Rv1 and PC3 cells transfected with the wild-type AR.

257 In PC3 cells transiently transfected with a luciferase repo

258 bal gene expression changes in JNK2-deprived PC3 cells using Serial Analysis of Gene Expression.

259 , both down-regulated survivin and decreased PC3 cell viability in serum-deprived conditions.

260 miR-182 expression in PC3 cells was also increased in response to stress induc

261 The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in

262 n of TMPRSS2-ERG in the gene fusion-negative PC3 cells was associated with the upregulation of wild-t

263 Receptor affinity (Kd) for human PC3 cells was determined using (99m)Tc-TP3939 and (64)Cu

264 Killing of PC3 cells was equivalent between the parental P/V-CPI(-)

265 Expression of GADD45alpha in PC3 cells was higher than that in Du145 and LNCaP cells

266 ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by gerany

267 lic stability was increased, and uptake into PC3 cells was proven without showing any intrinsic cytot

268 Release of ROS from prostate cancer (PC3) cells was studied using scanning electrochemical mi

269 NT (a prototypical component of CM) to treat PC3 cells, we found that the epidermal growth factor (EG

270 To find out the presence of invadopodia in PC3 cells, we performed a few comparative analyses with

271 PC3 cells, we propose, express a non-leukocyte-type, G p

272 ouse embryonic fibroblasts and p53/PTEN-null PC3 cells, we show that PTEN is more stable in p53-null

273 Using androgen-insensitive prostate cancer PC3 cells, we show that specific stimulation of endogeno

274 IC50 values in DU145, LNCaP, and PC3 cells were 50, 75, and 175 nM, respectively, for BI

275 p130CAS and paxillin activation in DU145 and PC3 cells were also inhibited.

276 PC3 cells were injected into the marrow of human fetal f

277 tion assays indicate that 12-LOX-transfected PC3 cells were more angiogenic than their neo controls.

278 However, DU145 and PC3 cells were more sensitive to 2-5A than LNCaP cells,

279 PTEN-negative PC3 cells were observed to have increased resistance to

280 were also observed when androgen-independent PC3 cells were treated with WIN-55,212-2 (5-30 microm).

281 n expression were stunted in CCL2-stimulated PC3 cells when treated either with the phosphatidylinosi

282 parthenolide further increases ROS levels in PC3 cells whereas it decreases radiation-induced oxidati

283 on of either Pak1 or Pak6 gene expression in PC3 cells, whereas protein levels of TGFbeta was elevate

284 However, in PC3 cells which produce and respond to IFN, the hyperfus

285 d apoptosis, we stably overexpressed PTEN in PC3 cells, which are prostate cancer cells that lack PTE

286 PC3 cells, which do not activate EGFR or Erk on LM5-rich

287 nsfection of a full-length hGCP II cDNA into PC3 cells, which do not express GCP II endogenously.

288 Only N-cadherin ligation in PC3 cells, which express both N-cadherin and E-cadherin,

289 PC3 cells, which express reduced ASS, also undergo autop

290 here was no binding to human prostate cancer PC3 cells, which lack PSMA, and binding was abolished by

291 nhibitors did not bind human prostate cancer PC3 cells, which lack PSMA, demonstrating specificity, a

292 stered tumor-cell colonies in coculture with PC3 cells, which might boost tumor stem-like properties.

293 after UV treatment in human prostate cancer PC3 cells, which possess mutant p53 with a truncated COO

294 sion, we generated stable 12-LOX-transfected PC3 cells, which synthesize high levels of 12-LOX protei

295 -incompetent mice bearing xenotransplants of PC3 cells with a combination of Wf-536 plus Marimastat w

296 Finally, restoration of AIF-deficient PC3 cells with AIF variants demonstrated that the enzyma

297 In vitro, co-culture of PC3 cells with bone tissue led to activation of pro-MMP-

298 sed significant effects on the cell cycle in PC3 cells, with the vast majority of treated cells in th

299 Expression of CSR1 in PC3 cell xenografts produced a dramatic reduction (>8-fo

300 Irradiation of PC3 cell xenografts that were treated with adenoviral EG