ライフサイエンスコーパス: prostate carcinoma cell

1 elial cells exert an anti-tumour activity on prostate carcinoma cells.

2 tal red fluorescent protein-expressing human prostate carcinoma cells.

3 ansmembrane collagen, collagen XXIII, in rat prostate carcinoma cells.

4 n of RASSF1A-expressing construct into LNCaP prostate carcinoma cells.

5 cycle progression and survival of human PC3 prostate carcinoma cells.

6 genes regulated by FKHRL1 and FKHR in LAPC4 prostate carcinoma cells.

7 owth factor (VEGF) expression in DU145 human prostate carcinoma cells.

8 oncosuppressive effect of DLC1 in metastatic prostate carcinoma cells.

9 and increases VEGF expression in DU145 human prostate carcinoma cells.

10 ulin-like growth factor (IGF)-1 signaling in prostate carcinoma cells.

11 rolled by translational efficiency in murine prostate carcinoma cells.

12 ated with high levels of HA synthesis by the prostate carcinoma cells.

13 ssion and its pro-survival response in human prostate carcinoma cells.

14 an (HA) pericellular matrix assembled on the prostate carcinoma cells.

15 looxygenase-2 (COX-2) inhibitor celecoxib in prostate carcinoma cells.

16 ontribute to preferential bone metastasis by prostate carcinoma cells.

17 U 145 human and metastatic MATLyLu (MLL) rat prostate carcinoma cells.

18 ongly suppresses the tumorigenicity of human prostate carcinoma cells.

19 ld increase in the invasive ability of human prostate carcinoma cells.

20 ional activity of AR in LNCaP and PC-3 human prostate carcinoma cells.

21 rilysin protein and mRNA expression in LNCaP prostate carcinoma cells.

22 gamma-glutamyl transpeptidase (GGT) in human prostate carcinoma cells.

23 ncrease GGT mRNA and protein levels in human prostate carcinoma cells.

24 ltures of bone marrow stromal cells with PC3 prostate carcinoma cells.

25 However, XMRV has not been found in prostate carcinoma cells.

26 - and for prostate precursor/stem cells and prostate carcinoma cells.

27 reased the HGF-driven motility of metastatic prostate carcinoma cells.

28 stimulates the intraosseous growth of PC-3M prostate carcinoma cells.

29 in androgen receptor-positive and -negative prostate carcinoma cells.

30 nd FB-Aca-BBN(7-14) was tested in PC-3 human prostate carcinoma cells.

31 ligand (TRAIL/Apo2-L)-mediated apoptosis in prostate carcinoma cells.

32 g pathway that controls the proliferation of prostate carcinoma cells.

33 tracellular HSP70 to the cell surface of the prostate carcinoma cells.

34 optosis particularly in androgen-independent prostate carcinoma cells.

35 sistance of the circulating metastatic human prostate carcinoma cells.

36 has antiproliferative consequences in LNCaP prostate carcinoma cells.

37 plex emerges as a new target of radiation in prostate carcinoma cells.

38 e of HSF1 in the malignant phenotype of PC-3 prostate carcinoma cells.

39 K1) in an HGF-dependent manner in metastatic prostate carcinoma cells.

40 ease of clusterin mRNA and protein levels in prostate carcinoma cells.

41 w this altered Ln-5 changes the migration of prostate carcinoma cells.

42 ethods to alleviate GSK-3beta suppression in prostate carcinoma cells.

43 ic survival after ionizing radiation (IR) of prostate carcinoma cells.

44 The murine prostate carcinoma cells 148-1,LMD and 148-1,PA were der

45 e epithelial cells (PZ-HPV-7); several human prostate carcinoma cells (22Rv1, DU145, LNCaP, and PC3);

46 In LNCaP prostate carcinoma cells, 5alpha-dihydrotestosterone ach

47 , we show that androgen deprivation of human prostate carcinoma cells activates the small GTPase, Ral

48 PN-1 levels increased in prostate carcinoma cells after downregulation of MMP-9 a

49 of wild-type p53 with increased survival of prostate carcinoma cells after fractionated exposure to

50 n were internalized by Siglec-XII-expressing prostate carcinoma cells, allowing targeting of a toxin

51 These data indicate that in human prostate carcinoma cells an inhibitor of the HMG-CoA red

52 ted the suppression of GSK-3beta activity in prostate carcinoma cells and enhanced the turnover of be

53 esions because of high expression of PSMA in prostate carcinoma cells and in bone metastases and lymp

54 (3-Cl-AHPC), induces apoptosis in breast and prostate carcinoma cells and inhibits AKT activity in th

55 First, using a series of human prostate carcinoma cells and normal human prostate epith

56 rmone-related protein (PTHrP) is produced by prostate carcinoma cells and tumors, but little is known

57 ressor virus replicates to greater levels in prostate carcinoma cells and, importantly, is a more pot

58 We show here that EGR1 binds to the AR in prostate carcinoma cells, and an EGR1-AR complex can be

59 MMP-9, highly invasive and metastatic human prostate carcinoma cells, androgen-repressed prostate ca

60 an +/-s.d.), and results in human breast and prostate carcinoma cell arrest and retention in the micr

61 Here, we used PC3M prostate carcinoma cells as a model to overexpress wild

62 Here, using PC3 human prostate carcinoma cells as a model, we provide direct e

63 in both human normal prostate epithelial and prostate carcinoma cells as well as in clinical prostate

64 CTL elicited by DC loaded with the PC3 prostate carcinoma cell bodies kill another prostate car

65 ing to induce AR-mediated gene activation in prostate carcinoma cells but also reveal the importance

66 ceptor 1 (FGFR1) is ectopically expressed in prostate carcinoma cells, but its functional contributio

67 egulation of NAG-1 expression in LNCaP human prostate carcinoma cells by 12-O-tetradecanoylphorbol-13

68 by MT1-MMP enhanced the migration of DU-145 prostate carcinoma cells by 2-fold compared with uncleav

69 MMP-9) activation promoted invasion of human prostate carcinoma cells by dissolving basement membrane

70 ndicate that EGCG induces apoptosis in human prostate carcinoma cells by shifting the balance between

71 nhibited the growth of poorly metastatic rat prostate carcinoma cells, causing cell cycle arrest in t

72 The growth of normal prostate as well as of prostate carcinoma cells depends on functional androgen

73 was observed in SUDHL4 cells, but not in PC3 prostate carcinoma cells despite comparable potency (SUD

74 n-tyrosine phosphatase, PTPmu, whereas LNCaP prostate carcinoma cells do not.

75 ines and corresponding mutations were: human prostate carcinoma cells DU-145/RC1 (mutation R364H), Ch

76 llular target for this class of drugs, human prostate carcinoma cells (DU-145) were made resistant to

77 stable maspin-expressing transfectants using prostate carcinoma cells DU145 as the parental cell line

78 In HCA7 colon and C4-2 prostate carcinoma cells, ERBB2 is constitutively activa

79 to identify gene expression changes in LNCaP prostate carcinoma cells exposed to PC-SPES and estrogen

80 We also found that the prostate carcinoma cells expressing high levels of MT1-M

81 Unlike control tumors, tumors of rat prostate carcinoma cells expressing recombinant sNRP1 we

82 l, expression of functional bcl-2 protein in prostate carcinoma cells failed to signal protection aga

83 ilencing in vitro and extend tests to target prostate carcinoma cells following systemic administrati

84 ditional PLCgamma1 knockdown in PC3LN3 human prostate carcinoma cells for further evaluation of PLCga

85 vivo, and in vivo that metastatic breast and prostate carcinoma cells form multicellular homotypic ag

86 Etk pathway is involved in the protection of prostate carcinoma cells from apoptosis in response to P

87 of highly malignant viable circulating human prostate carcinoma cells from orthotopic but not ectopic

88 d hormone-related protein) overexpression by prostate carcinoma cells has been implicated in tumor pr

89 s in various malignant cells including human prostate carcinoma cells (HPC).

90 ial dilution experiments, PTI-1 can detect 1 prostate carcinoma cell in 10(8) cells not expressing PT

91 vo model of NI was established by implanting prostate carcinoma cells in the sciatic nerves of nude m

92 e molecules in the death of the DU-145 human prostate carcinoma cells induced by methylseleninic acid

93 ous than sequential treatment in human DU145 prostate carcinoma cells infected with an adenovirus con

94 ostate tumor growth and drastically enhances prostate carcinoma cell interaction with surrounding str

95 density the migration speed of DU-145 human prostate carcinoma cells is a balance between tractile a

96 show that N-cadherin mRNA expression in PC-3 prostate carcinoma cells is dependent on beta(1) integri

97 Because the growth of human prostate carcinoma cells is influenced by androgens and/

98 ven by the CDKN1A and CDH1 promoters in PC-3 prostate carcinoma cells is sensitive to treatment with

99 transfection prevented the proliferation of prostate carcinoma cells, led to lactate dehydrogenase r

100 NA in a breast cancer cell line (MCF7) and a prostate carcinoma cell line (DU145).

101 hr7 or hchr12 into a highly aggressive human prostate carcinoma cell line (PC3) by microcell-mediated

102 ng cancer (H69) cell lines or a variant of a prostate carcinoma cell line (PC3-N).

103 owing, anaplastic variant of the Dunning rat prostate carcinoma cell line (R3327-AT) was implanted su

104 In this report, we characterized the human prostate carcinoma cell line 22Rv1 in an orthotopic syst

105 sion, using as our model the PA DU-145 human prostate carcinoma cell line and a highly invasive subli

106 excellent in vitro uptake within the DU-145 prostate carcinoma cell line and orthotopically implante

107 Xenograft tumors of prostate carcinoma cell line DU 145 and hepatocarcinoma

108 le of prostate cancer cells, using the human prostate carcinoma cell line DU145 that has mutations in

109 (223Leu) and p53(274Phe), from Fas-resistant prostate carcinoma cell line DU145.

110 acellular Ca2+ was examined in the Dunning G prostate carcinoma cell line following apoptosis inducti

111 ma incidence, restoration of expression in a prostate carcinoma cell line homozygous for the frameshi

112 at the PEITC-induced apoptosis in PC-3 human prostate carcinoma cell line is mediated by ERKs.

113 lating factor (GM-CSF) receptor in the human prostate carcinoma cell line LNCaP and looked for its pr

114 f androgen-stimulated and unstimulated human prostate carcinoma cell line LNCaP identified androgen i

115 he level of expression of Bcl-2 in the human prostate carcinoma cell line LNCaP observed in response

116 erse transcription-PCR from the PSM-positive prostate carcinoma cell line LNCaP.

117 d differential display analysis of the human prostate carcinoma cell line PC-3 and its highly metasta

118 sed in many cancers including the metastatic prostate carcinoma cell line PC-3-M.

119 elial growth factor (VEGF) in vitro in human prostate carcinoma cell line PC-3.

120 prostate carcinoma cell bodies kill another prostate carcinoma cell line, DU145, suggesting recognit

121 rexpression of FGF8b in a weakly tumorigenic prostate carcinoma cell line, LNCaP, could alter the gro

122 In the DU-145 prostate carcinoma cell line, rhIL-11 stimulates a trans

123 t activated by PEITC treatment in PC-3 human prostate carcinoma cell line.

124 wth arrest in PC-3-M cells, a p53-null human prostate carcinoma cell line.

125 ) disseminating variants from the human PC-3 prostate carcinoma cell line.

126 l and apoptotic responses in the NRP-154 rat prostate carcinoma cell line.

127 Utilizing prostate carcinoma cell lines (C1, C2, and C3) derived f

128 ave observed HSP70 release from intact human prostate carcinoma cell lines (PC-3 and LNCaP) by a mech

129 We now demonstrate that human prostate carcinoma cell lines (PC-3, DU-145, and LN-CaP)

130 ssion of N-cadherin in poorly differentiated prostate carcinoma cell lines (PC-3N derived from PC-3,

131 ecreted MDA-7/IL-24 in inducing apoptosis in prostate carcinoma cell lines and displayed transformed

132 nantly expressed only in N-cadherin-positive prostate carcinoma cell lines and prostate stromal fibro

133 consequences of L-plastin down-regulation in prostate carcinoma cell lines by both transfection and r

134 plastin expression is also detected in other prostate carcinoma cell lines by reverse transcriptase p

135 We show here in both pancreatic and prostate carcinoma cell lines cobalt chloride (used to m

136 C-3) versus metastatic variant (PC-3M) human prostate carcinoma cell lines led to identification of t

137 s expressed differentially between the human prostate carcinoma cell lines LNCaP and PC-3, which are

138 tion of this cyclase was investigated in the prostate carcinoma cell lines LNCaP and PC3.

139 ion of Hsp72 did not reduce viability of the prostate carcinoma cell lines PC-3 and DU-145.

140 of the E-cadherin/catenin phenotype of human prostate carcinoma cell lines showed loss of E-cadherin

141 -cadherin and loss of E-cadherin by invasive prostate carcinoma cell lines suggests a progression fro

142 tructural characteristics of four human PC-3 prostate carcinoma cell lines transduced with C-CAM1 ret

143 We have shown previously that the putative prostate carcinoma cell lines TSU-Pr1 and JCA-1 share a

144 d the role of FAK in regulating migration of prostate carcinoma cell lines with increasing metastatic

145 ibitor, significantly inhibited migration of prostate carcinoma cell lines, demonstrating that tumor

146 ates tumor metastasis, we used two different prostate carcinoma cell lines, DU145 and PC3, in which t

147 We examined the effects of 4-HPR on two prostate carcinoma cell lines, LNCaP (an androgen-sensit

148 Introduction of either constructs into prostate carcinoma cell lines, PC-3 and its isogenic but

149 Recombinant hK2 was also expressed in human prostate carcinoma cell lines, PC3 (PC3-hK2) and DU145 (

150 kDa PRL transfection in DU145 and PC-3 human prostate carcinoma cell lines, we demonstrated that expr

151 1A promoter was observed in five widely used prostate carcinoma cell lines, which acquired the abilit

152 silencing of RASSF1A was found in four other prostate carcinoma cell lines, which were adapted for ce

153 of human prostate tumors, mouse tumors, and prostate carcinoma cell lines.

154 ombination of PB and CRA on human and rodent prostate carcinoma cell lines.

155 he expression of E- versus N-cadherin by the prostate carcinoma cell lines.

156 tivities against LNCaP, DU145, and PC3 human prostate carcinoma cell lines.

157 protein and O-GlcNAc levels are elevated in prostate carcinoma cell lines.

158 Here, we report that prostate carcinoma cells LNCaP and PC3 autoactivate late

159 tosterone-mediated induction of ODC in human prostate carcinoma cells, LNCaP as an in vitro model, an

160 Preferential bone metastasis of prostate carcinoma cells may therefore be facilitated by

161 Prostate carcinoma cells metastasizing to bone must init

162 transfection and treatment on production by prostate carcinoma cells of IL (interleukin)-8, which ca

163 Therefore, expression of PARP-DBD in prostate carcinoma cells offers a strategy to achieve se

164 to that shown by the apoptosis-resistant PC3 prostate carcinoma cells only after 3,000 nmol/L for 48

165 Human prostate carcinoma cells (PC-3) release enzymatic activi

166 oration of CEACAM1(a)-4L expression in human prostate carcinoma cells (PC-3) suppresses tumorigenicit

167 ls (PrECs) compared with their expression in prostate carcinoma cells (PC-3).

168 c approach and generated an isogenic pair of prostate carcinoma cells PC3 (p53-/-) by stably introduc

169 Fas expression and converting Fas-sensitive prostate carcinoma cells PC3 into Fas-resistant ones.

170 NV1023 had significant oncolytic effect on prostate carcinoma cells (PC3, DU145, and LNCap) in vitr

171 Here we show that 22Rv1 prostate carcinoma cells produce high-titer virus that i

172 F4/p130 association after IR was observed in prostate carcinoma cells regardless of their sensitivity

173 SRB12-p9 skin SCC cells, as well as with PC3 prostate carcinoma cells, revealed that RXRalpha transcr

174 r prostate stromal cells cotransplanted with prostate carcinoma cells s.c. into nude mice reduced tum

175 Here we show that the metastatic human prostate carcinoma cells selected for survival in the ci

176 TGFbeta and the medium conditioned by the prostate carcinoma cells stimulated myofibroblast differ

177 s increased and accumulated in the nuclei of prostate carcinoma cells subjected to ionizing radiation

178 r data demonstrate an important role for the prostate carcinoma cell surface in mediating the inhibit

179 Here we report that in AT-3 prostate carcinoma cells, SV infection decreases superox

180 d receptor expressed at the surface of human prostate carcinoma cells that plays central roles in ang

181 The present study shows that in prostate carcinoma cells, the mda-7/IL-24-induced ER str

182 verexpressed in estramustine resistant human prostate carcinoma cells, these results indicate that be

183 y be responsible for enhanced sensitivity of prostate carcinoma cells to a variety of anticancer trea

184 cells to proteasome and Hsp90 inhibitors and prostate carcinoma cells to proteasome inhibitors.

185 sitized the apoptotic response of breast and prostate carcinoma cells to various drugs, ranging from

186 odel showed that some rapidly promoted LNCaP prostate carcinoma cell tumorigenesis and others had no

187 omote angiogenesis and growth of LNCaP human prostate carcinoma cell tumors, and that these increases

188 Par-4 was first isolated from prostate carcinoma cells undergoing apoptosis, and expre

189 SAT was conditionally overexpressed in LNCaP prostate carcinoma cells via a tetracycline-regulatable

190 uced IkappaBalpha degradation in human LNCaP prostate carcinoma cells, we observed that persistent in

191 Alone, LNCaP prostate carcinoma cells were essentially nontumorigenic

192 In contrast, highly metastatic prostate carcinoma cells were resistant to the growth in

193 ydrazine (laromustine)-resistant DU145 human prostate carcinoma cells, which express high levels of A

194 CTL elicited by DC loaded with killed LNCap prostate carcinoma cells, which express prostate specifi

195 Breast and prostate carcinoma cells with activated PI(3) kinase los

196 Treatment of T24 bladder and PC3 prostate carcinoma cells with full-length and 3'-truncat

197 as well as the effects of depleting Pim1 in prostate carcinoma cells with high levels of MYC.

198 Conversely, breast and prostate carcinoma cells with minimal PI(3) kinase activ

199 Treatment of prostate carcinoma cells with the novel retinoid 6-[3-(1

200 In PC-3 prostate carcinoma cells (with overexpression of Bcl-2),

201 n specifically induced in vitro apoptosis in prostate carcinoma cells, with innate resistance to chem