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1 nscript A-to-I editing detected in DU145 and PC3 cells.
2 gests that more than one step is affected in PC3 cells.
3 y different RNA editing enzymes in DU145 and PC3 cells.
4 viral replication cycle that is inhibited in PC3 cells.
5 e cancer LNCaP and its derivative C4-2B, and PC3 cells.
6 yxin formed a complex with ezrin in MCF7 and PC3 cells.
7 uction in LNCaP cells but only low levels in PC3 cells.
8 ls as compared with control mock-transfected PC3 cells.
9 pression was much lower than that of control PC3 cells.
10 to selenite-induced apoptosis than p53-null PC3 cells.
11 as maspin siRNA decreased CK18 expression in PC3 cells.
12 ibitory effects on migration and invasion of PC3 cells.
13 l cancer KYSE 150 cells, and prostate cancer PC3 cells.
14 an localize to the nucleus in both DU145 and PC3 cells.
15 eactivity to other family members in HeLa or PC3 cells.
16 sensitivity to UV than observed in wild-type PC3 cells.
17 lowing UV treatment and shown to increase in PC3 cells.
18 d-p53 in both control and bcl-2-transfectant PC3 cells.
19 nce was observed in 22Rv1, DU145, LNCaP, and PC3 cells.
20 the down-regulation of Cdc6 transcription in PC3 cells.
21 as the serine peptidases CTSA and SCPEP1, in PC3 cells.
22 drogen-independent metastatic human prostate PC3 cells.
23 te cancer cells, including DU145, LNCaP, and PC3 cells.
24 ecules are detected, especially in DU145 and PC3 cells.
25 issue-specific colonization of human bone by PC3 cells.
26 served in the tumors from 12-LOX-transfected PC3 cells.
27 1,25D(3)-induced CYP24A1 mRNA expression in PC3 cells.
28 ndogenous CYP24A1 mRNA level in TBBz-treated PC3 cells.
29 , colon cancer HCT116 and prostate carcinoma PC3 cells.
30 an increased uptake of W106F-cystatin C, in PC3 cells.
31 caspase-9 but not caspase-3 was activated in PC3 cells.
32 ation to the protein expression in LnCAP and PC3 cells.
33 d to be potential target genes of miR-182 in PC3 cells.
34 duce integrin activity and cell migration in PC3 cells.
35 SubA has no effect on Hep3B and PC3 cells.
36 orthotopic implantation of DsRed-expressing PC3 cells.
37 ormation of peripheral adhesion complexes in PC3 cells.
38 ve in suppressing the growth and motility of PC3 cells.
39 protein in RWPE-1 and DU145 cells but not in PC3 cells.
40 ctin- and dynamin-dependent pathway to enter PC3 cells.
41 sed glycerophosphocholine and tCho levels in PC3 cells.
42 is markedly reduced when Pin1 is depleted in PC3 cells.
43 tion and metastasis seen in mock-transfected PC3 cells.
44 is critical for anticancer activity against PC3 cells.
45 effect on proliferation of prostate cancer (PC3) cells.
46 androgen receptor-negative prostate cancer (PC3) cells.
49 CAP cells as well as in androgen-independent PC3 cells abrogates DHT- and/or EGF-induced Erk signalin
50 ere solely arrested in mitosis on treatment, PC3 cells accumulated in G2 phase and mitosis, suggestin
56 al PI3K activity was mediated by p110beta in PC3 cells and by both p110beta and p110delta in LNCaP ce
57 osis in androgen-independent prostate cancer PC3 cells and compared its effect with that of staurospo
59 the myosin phosphatase was phosphorylated in PC3 cells and HUVECs, and phosphorylation of MYPT1 and t
62 unx2 and Fra-2 are higher in the OC-positive PC3 cells and osteoblasts, compared with the OC-negative
63 and gelatinolytic activity as compared with PC3 cells and PC3 cells expressing mutant OPN in integri
65 er, the increased cell proliferation rate of PC3 cells and TREK-1 overexpressing CHO cells could be r
66 sie Blue-stained band) was down-regulated in PC3 cells and up-regulated in KB cells after UV exposure
67 a tissues, 15-LOX-2 mRNA was not detected in PC3 cells, and they did not produce detectable 15-HETE f
68 ibody to alpha(v)beta(5) (and in the case of PC3 cells, anti-alpha(v)beta(3)) resulted in significant
69 ycle arrest with decline in CDK1 activity in PC3 cells, apoptosis of SUDHL4 cells occurred without ev
76 and longer doubling time of MBP-1 knockdown PC3 cells as compared with control mock-transfected PC3
77 own of PIP5K1alpha exerts similar effects on PC3 cells as ISA-2011B treatment, significantly inhibiti
80 jugates selectively adhered to LNCaP but not PC3 cells at static and low shear (<1 dyn/cm2) but not h
83 in vitro, and in vivo shRunx2 expression in PC3 cells blocked their ability to survive in the bone m
84 Im inhibited the cell viability of DU145 and PC3 cells but did not affect the viability of fibroblast
85 that the p53R2 binding to hRRM1 decreased in PC3 cells but increased in KB cells after UV treatment.
87 radiosensitization effect on prostate cancer PC3 cells but not on normal prostate epithelial PrEC cel
89 oss of viability of the human tumor HeLa and PC3 cells, but the coadministration of copper increases
90 nsible for the high hOC promoter activity in PC3 cells by binding to the OSE2, AP-1/VDRE, and OSE1 el
91 c expression of c-FLIP(L) in TRAIL-sensitive PC3 cells changed their phenotype from TRAIL sensitive t
94 sion showed that in contrast to LNCaP cells, PC3 cells constitutively expressed numerous antiviral ge
97 r shown to exhibit increased cytotoxicity in PC3 cell culture medium that was already below pH 7.0 at
102 erin-11 in cadherin-11-expressing metastatic PC3 cells decreases cell motility and invasiveness.
103 cating that metastatic human prostate cancer PC3 cells deficient in DAB2IP (shDAB2IP) exhibit increas
105 Ribozyme suppression of MMP-9 expression in PC3 cells did not affect pro-MMP-9 activation or net MMP
108 d with the control clones, HOXB13-expressing PC3 cells exhibited significant inhibition of in vitro a
111 the human prolactin receptor, but DU145 and PC3 cells express only low amounts of this receptor unti
113 inoculation into the prostate of nude mice, PC3 cells expressing core3 O-glycans produced much small
115 ctivated cell sorter analysis suggested that PC3 cells expressing MBP-1-specific small interfering RN
116 ytic activity as compared with PC3 cells and PC3 cells expressing mutant OPN in integrin-binding doma
118 cancer cell line (PC3) that lacks Stat3 and PC3 cells expressing wild-type Stat3 or a Stat3 mutant c
120 n into athymic nude mice, 12-LOX-transfected PC3 cells formed larger tumors than did the controls.
121 indicate that CCL2 protects prostate cancer PC3 cells from autophagic death via the phosphatidylinos
122 onstrates that CCL2 protects prostate cancer PC3 cells from autophagic death, allowing prolonged surv
123 ecific knockdown of ALCAM in bone-metastatic PC3 cells greatly diminished both skeletal dissemination
124 erestingly, AR gene transcripts in DU145 and PC3 cells harbored a large number of single base pair nu
125 ve clinical disease; (2) ERK5-overexpressing PC3 cells have enhanced proliferative, migrative and inv
128 ced apoptosis and inhibited proliferation of PC3 cells in culture, but both MDM2 overexpression and k
129 nant LOX-PP (rLOX-PP) inhibits the growth of PC3 cells in vitro by mechanisms that were not character
130 d the invasive phenotype in SPDEF expressing PC3 cells in vitro, suggesting that the effects of SPDEF
131 , restoration of wild-type p53 expression in PC3 cells increased cellular sensitivity to selenite and
133 EphA2 phosphorylation and cells rounding in PC3 cells, indicating EphA2-antagonizing activity of EM2
134 small interfering RNA kills prostate cancer PC3 cells, indicating that the TGFbeta2-NF-kappaB pathwa
135 Coculturing RhoA knockout fibroblasts and PC3 cells induced expression of proinflammatory genes in
137 Invadopodia enable polarized invasion of PC3 cells into the gelatin matrix in a time-dependent ma
138 alectin-3 knockdown in human prostate cancer PC3 cells led to cell-cycle arrest at G(1) phase, up-reg
140 cluding c-myc were overexpressed in both the PC3 cell line and DU145, but the PC3 to DU145 expression
141 transfection of a full-length cDNA into the PC3 cell line confers NAAG-hydrolyzing activity that is
142 In addition, loss of RalA in the metastatic PC3 cell line inhibited bone metastasis but did not affe
143 pase cleavage in the prostate cancer-derived PC3 cell line is metabolically unstable in cells because
144 ppression of PS1 expression in p53-deficient PC3 cell line suggesting that inhibition of basal JNK ac
145 the function of TARP, we generated a stable PC3 cell line that expresses TARP in a constitutive mann
146 LNCaP cell line and the androgen-insensitive PC3 cell line to treatment with the topoisomerase I inhi
147 The highly invasive human prostate cancer PC3 cell line was found to express the alpha(v)beta3 int
149 is down-regulated in the highly tumorigenic PC3 cell line, which suggests that, in addition to its f
152 ated enhanced cytotoxicity against 4T1.2 and PC3 cell lines compared to DOX and DOX-loaded POEG-b-PCC
153 is of gene expression from treated DU145 and PC3 cell lines demonstrate a close similarity of nelfina
154 ess conditions, AIF depletion from DU145 and PC3 cell lines led to significant reductions in cell sur
158 ortmannin, a PI 3-kinase inhibitor, prevents PC3 cell migration on both osteopontin and vitronectin;
159 of Pak1, and not Pak6, resulted in impaired PC3 cell migration, the effects of Pak1 knockdown on tra
160 hat such activation was required for maximal PC3 cell mitogenesis, as measured by 5-bromo-2'-deoxy-ur
161 ly showed jumps in their force curves, while PC3 cells on bovine-serum-albumin- and antibody-treated
163 n of platelet-type 12-LOX in prostate cancer PC3 cells or epithelial cancer A431 cells significantly
164 tly, holoclones derived from either cultured PC3 cells or holoclone-initiated tumors can be serially
165 demonstrated that restoring AR in epithelial PC3 cells or knockdown of AR in stromal WPMY1 cells supp
166 mutant forms of EGFR (Tyr(845)) or Stat5b in PC3 cells, or treatment with selective, catalytic inhibi
172 r resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulatio
174 s study, we found that PDGF-D-overexpressing PC3 cells (PC3 cells stably transfected with PDGF-D cDNA
175 B1 expression was observed in MBP-1-depleted PC3 cells (PC3-4.2) upon serum stimulation, although the
178 ein was no longer effective in up-regulating PC3 cell proliferation, invasion, and MMP-9 activation,
180 dentified in co-culture studies showing that PC3 cells promote osteoclastogenesis and inhibit osteobl
185 ADAR1 and ADARB1 were observed in DU145 and PC3 cells relative to the androgen-responsive LNCaP and
186 utamide via a cleavable linear tether enters PC3 cells, resides in cytosol, binds to the AR if presen
188 blot analysis revealed that PFE treatment of PC3 cells resulted in (i) induction of Bax and Bak (proa
189 atment to human PCa LNCaP, C4-2, 22Rnu1, and PC3 cells resulted in a dose-dependent inhibition of cel
190 t of highly aggressive human prostate cancer PC3 cells resulted in a dose-dependent inhibition of cel
191 data demonstrated that uPA-uPAR knockdown in PC3 cells resulted in a dramatic reduction of tumor cell
193 weekly) to athymic nude mice implanted with PC3 cells resulted in a significant inhibition of tumor
194 The induced expression of GPx3 in DU145 and PC3 cells resulted in an increase in reactive oxygen spe
195 h its role in invasion, depletion of CD97 in PC3 cells resulted in decreased bone metastasis without
196 of JunD expression using siRNA in DU145 and PC3 cells resulted in significant reduction in cell prol
197 Ectopic expression of TMEFF2 in DU145 and PC3 cells resulted in their prominent inhibition of grow
198 ansfection of ERK5wt and MEK5D constructs in PC3 cells results in predominant ERK5 nuclear localizati
201 -catenin was re-introduced, the phenotype of PC3 cells reverted back to a more epithelial phenotype w
202 thraquinone fluorescence of targeted drug in PC3 cells showed initial cytosolic localization, indepen
204 d PC3-TR (a TRAIL-resistant subpopulation of PC3) cells showed increased c-FLIP(L) mRNA levels and ma
205 ble upregulation of TSPAN1 in both DU145 and PC3 cells significantly increased cell migration and ind
206 ic expression of miR-182 and miR-141/200a in PC3 cells significantly reduced protein levels, GNA13-3'
207 and silibinin in human prostate cancer (PCA) PC3 cells; silymarin is comprised of silibinin and its o
209 lular delivery was tested in GRPR expressing PC3 cells stably transfected with a luciferase gene inte
210 found that PDGF-D-overexpressing PC3 cells (PC3 cells stably transfected with PDGF-D cDNA and referr
211 roscopy, which showed a higher percentage of PC3 cells staining positive for P-S319-Runx2 relative to
213 PUMA in response to 3beta-Adiol in LNCaP and PC3 cells, suggesting that FOXO3a mediates the apoptotic
214 as EGF-induced cyclin D1 mRNA expression in PC3 cells, suggesting that paxillin may regulate prostat
216 rved higher degrees of ROS generation in the PC3 cells than DU145 and LNCaP, and that ROS generation
221 which harbor the TMPRSS2-ERG gene fusion and PC3 cells that stably express a similar construct (fusio
222 vation of MAPK and PI3K activity in MCF7 and PC3 cells through its ability to form a complex with ezr
223 in the process of migration and invasion of PC3 cells through regulating processes essential for the
224 st that mevastatin inhibits cdk2 activity in PC3 cells through the inhibition of Thr-160 phosphorylat
225 Like DHA, the DHA metabolites a) induce PC3 cells to activate a peroxisome proliferator-activate
227 potently sensitizes radioresistant LNCaP and PC3 cells to gamma radiation, regardless of the status o
230 LOX-PP was shown to sensitize both DU145 and PC3 cells to radiation-induced cell death determined in
232 tion of JNK is required for sensitization of PC3 cells to TRAIL-induced apoptosis by translation inhi
234 boxypeptidase were expressed in membranes of PC3 cells transfected with either pig folylpoly-gamma-ca
235 -induced gene activation was also present in PC3 cells transfected with the AR but not in the parenta
238 bal gene expression changes in JNK2-deprived PC3 cells using Serial Analysis of Gene Expression.
241 The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in
242 n of TMPRSS2-ERG in the gene fusion-negative PC3 cells was associated with the upregulation of wild-t
248 NT (a prototypical component of CM) to treat PC3 cells, we found that the epidermal growth factor (EG
249 To find out the presence of invadopodia in PC3 cells, we performed a few comparative analyses with
251 ouse embryonic fibroblasts and p53/PTEN-null PC3 cells, we show that PTEN is more stable in p53-null
252 Using androgen-insensitive prostate cancer PC3 cells, we show that specific stimulation of endogeno
256 tion assays indicate that 12-LOX-transfected PC3 cells were more angiogenic than their neo controls.
259 were also observed when androgen-independent PC3 cells were treated with WIN-55,212-2 (5-30 microm).
260 n expression were stunted in CCL2-stimulated PC3 cells when treated either with the phosphatidylinosi
261 parthenolide further increases ROS levels in PC3 cells whereas it decreases radiation-induced oxidati
262 on of either Pak1 or Pak6 gene expression in PC3 cells, whereas protein levels of TGFbeta was elevate
264 d apoptosis, we stably overexpressed PTEN in PC3 cells, which are prostate cancer cells that lack PTE
266 nsfection of a full-length hGCP II cDNA into PC3 cells, which do not express GCP II endogenously.
269 here was no binding to human prostate cancer PC3 cells, which lack PSMA, and binding was abolished by
270 nhibitors did not bind human prostate cancer PC3 cells, which lack PSMA, demonstrating specificity, a
271 stered tumor-cell colonies in coculture with PC3 cells, which might boost tumor stem-like properties.
272 after UV treatment in human prostate cancer PC3 cells, which possess mutant p53 with a truncated COO
273 sion, we generated stable 12-LOX-transfected PC3 cells, which synthesize high levels of 12-LOX protei
274 -incompetent mice bearing xenotransplants of PC3 cells with a combination of Wf-536 plus Marimastat w
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