ライフサイエンスコーパス: sarcoma cell

1 tors (TFs): KLF15, TCF4 and NKX2-2, in Ewing sarcoma cells.

2 diated nude mice before injection of Ewing's sarcoma cells.

3 and selectively blocks the survival of bone sarcoma cells.

4 derived from the Engelbreth-Holm-Swarm mouse sarcoma cells.

5 d confirmed these results in HH-driven Ewing sarcoma cells.

6 L-4 gag), D5 mouse melanoma, or MCA304 mouse sarcoma cells.

7 ding (pnc) transcript, is expressed in Ewing sarcoma cells.

8 sensitizes DOX-induced cell killing in human sarcoma cells.

9 breast cancer cells or KS1767 human Kaposi's sarcoma cells.

10 esenchymal progenitor cells (MPCs) and Ewing sarcoma cells.

11 breast cancer, RKO colon cancer, and SAOS-2 sarcoma cells.

12 l types, including acute leukemia and Kaposi sarcoma cells.

13 he motility stimulation of human soft tissue sarcoma cells.

14 py of metastasis induced by wild-type Ag104A sarcoma cells.

15 t but did not activate apoptosis in p53(-/-) sarcoma cells.

16 hydrogel produced from Engelbreth-Holm-Swarm sarcoma cells.

17 ibiting calcium transporters radiosensitized sarcoma cells.

18 blocked in vitro and in vivo growth of Ewing sarcoma cells.

19 lysis in MiaPaCa2 pancreatic cancer and A673 sarcoma cells.

20 , thereby inducing an IFN signature in Ewing sarcoma cells.

21 antibody conjugated with drugs to kill Ewing sarcoma cells.

22 erence inhibited oncogenic activity in Ewing sarcoma cells.

23 s and metastatic potential of non-epithelial sarcoma cells.

24 inhibits the transformed phenotype of Ewing sarcoma cells.

25 also in the differential phenotype of Ewing sarcoma cells.

26 to be critical for proliferation of Ewing's sarcoma cells.

27 nifest growth inhibitory properties in Ewing sarcoma cells.

28 in vitro dose of 4- or 9-Gy irradiation, KP sarcoma cells acquire mutational neoantigens and become

29 Fas ligand could only be detected in Ewing's sarcoma cells after permeabilization.

30 In sarcoma cells alone, peptides corresponding to 39 tyrosi

31 ata from a genome-wide shRNA screen in Ewing sarcoma cells also identified the proteasome as a node o

32 genesis activators and mitogens for Kaposi's sarcoma cells and B cells.

33 fied by hypoxia-induced PLOD2 is secreted by sarcoma cells and binds to integrin beta1 on endothelial

34 ein-alpha (FAP) is often highly expressed by sarcoma cells and by sarcoma-associated fibroblasts in t

35 entify the circRNAs expressed in soft tissue sarcoma cells and explore how the circRNAs regulate sarc

36 Expression of EWSR1-FLI1 in non-Ewing sarcoma cells and in MPCs enhances FATE1 mRNA and protei

37 ient transfection experiments in rat chondro-sarcoma cells and in NIH-3T3 fibroblasts demonstrated th

38 ion of LDHA inhibited proliferation of Ewing sarcoma cells and induced apoptosis, phenocopying pharma

39 expression of the flt-4 receptor in Kaposi's sarcoma cells, and double labeling revealed its colocali

40 ncer cell lines (MC3T3-E1 osteoblasts, MG-63 sarcoma cells, and MDA-MB-231 breast cancer cells) confi

41 formation leaves a single EWS allele in the sarcoma cells, and the contribution that the loss of EWS

42 to various subcellular compartments of mouse sarcoma cells, and the resulting cells were tested for p

43 rmine the expression and function of DDX3 in sarcoma cells, and to investigate the antitumor activity

44 demonstrate, for the first time, that Ewing sarcoma cells are exquisitely sensitive to inhibition of

45 We show that mouse and human synovial sarcoma cells are sensitive in vitro to ABT-263, a BH3-p

46 of tumor suppression was validated in Ewing sarcoma cells, B-cell tumors, and human keratinocytes wh

47 93T:A mtDNA in both lung carcinoma and osteo-sarcoma cell backgrounds.

48 r inhibiting its kinase activity in synovial sarcoma cells blocked rapamycin-induced phosphorylation

49 ography) reflects EWS-FLI1 activity in Ewing sarcoma cells both in vitro and in vivo.

50 ligase that is highly expressed in synovial sarcoma cells but relatively underexpressed in human iPS

51 susceptibility and rejection of transfected sarcoma cells by immunocompetent animals.

52 Induction of apoptosis in Ewing's sarcoma cells by ionizing radiation is accompanied by ac

53 d in primary fibroblasts and U2OS osteogenic sarcoma cells by treatment with small molecule Cdk inhib

54 of the arrest, we generated U2-OS osteogenic sarcoma cell clones in which p16 transcription could be

55 We explored this issue using osteogenic sarcoma cell clones with inducible p16INK4a expression.

56 itro, and genetic silencing of ASNS in mouse sarcoma cells combined with depletion of plasma asparagi

57 mutant mdr1 gene into drug-sensitive MES-SA sarcoma cells confers resistance to both doxorubicin and

58 The introduction of wt p53 into sarcoma cells containing mutant p53 significantly reduce

59 We observed that Ewing sarcoma cells cultured in porous 3D electrospun poly(eps

60 Interestingly, in Ewing sarcoma cells, DKK2 suppression simultaneously increased

61 YB-1 inactivation in human sarcoma cells dramatically reduces G3BP1 and SG formatio

62 gradient accurately, we examined individual sarcoma cells embedded in the O2-controllable hydrogel.

63 Sarcoma cells exposed to sublethal doses of fentomycin-1

64 therapies, we assessed the tumorigenicity of sarcoma cells expressing combinations of class II, Ii, a

65 similar suppression of apoptosis in Ewing's sarcoma cells expressing EWS-Fli-1 and EWS-erg proteins

66 ells expressing wt p53 compared with CM from sarcoma cells expressing mutant p53.

67 wt p53 compared with CM from human synovial sarcoma cells expressing mutant p53.

68 The growth of MCA sarcoma cells expressing the intron-derived SL8 epitope

69 conditioned medium (CM) from human synovial sarcoma cells expressing wt p53 compared with CM from hu

70 creased when cells were treated with CM from sarcoma cells expressing wt p53 compared with CM from sa

71 Using SYN-1 sarcoma cells, FMSF predominantly stimulated chemotaxis

72 ng PI3K and PKCs is important for protecting sarcoma cells from rapamycin-induced apoptosis.

73 -mediated knockdown of Mekk3 in TC71 Ewing's sarcoma cells had no effect on tumor growth or vessel de

74 including the marked sensitivity of Ewing's sarcoma cells harbouring the EWS (also known as EWSR1)-F

75 synthesis and inhibited the growth of Ewing sarcoma cells in vitro and in vivo in a xenograft.

76 naling and decreases tumorigenicity of Ewing sarcoma cells in vitro and in vivo.

77 the SIRT1/2 inhibitor Tenovin-6 killed Ewing sarcoma cells in vitro and prohibited tumor growth and s

78 killed NGFR-(b)CD- and NGFR-(y)CD-transduced sarcoma cells in vitro through direct and bystander effe

79 rigelTM) by NIH 3T3, mouse fibrosarcoma, and sarcoma cells in vitro, but it has no such effect on lym

80 (Fluorescence microscopy and ELISA) in MG63 sarcoma cells in vitro.

81 efficiently killed allogeneic and autologous sarcoma cells in vitro.

82 t with RK-33 was preferentially cytotoxic to sarcoma cells, including chemotherapy-resistant Ewing sa

83 nd it was chemotactic for a variety of human sarcoma cells, including fibrosarcoma, leiomyosarcoma, l

84 somerase IIalpha expression in human Ewing's sarcoma cells, increasing their apoptosis rate and enhan

85 This work extends our previous study(1) that sarcoma cells injected intravenously form intravascular

86 on did not alter the metastatic potential of sarcoma cells injected orthotopically, but the simultane

87 tumors and the differentiation of osteogenic sarcoma cells into mature osteocytes.

88 after intramedullary injection of osteolytic sarcoma cells into the femur, there was extensive bone d

89 report the impact of hypoxic O2 gradients on sarcoma cell invasion and migration.

90 antitumor effect of wt p53 overexpression in sarcoma cells is attributable not only to enhanced cell

91 s is by endocytosis, whereas entry in rat XC sarcoma cells is by surface fusion.

92 c expression of miR-483-5p in IGF2-dependent sarcoma cells is correlated with increased tumorigenesis

93 Rapamycin-induced apoptosis in sarcoma cells is inhibited by insulin-like growth factor

94 WT1 expression in Ewing sarcoma cells is up-regulated by hypoxia.

95 However, in some Kaposi sarcoma cells, KSHV undergoes a productive life cycle an

96 Conversely, depletion of EWSR1-FLI1 in Ewing sarcoma cells leads to a loss of FATE1 expression.

97 transduction, we engineered a parental human sarcoma cell line (2C4) as well as sarcoma cell lines th

98 osed of a low MDR1-expressing parent uterine sarcoma cell line and a daughter cell line selected for

99 Research has been hampered by limited human sarcoma cell line availability and the large number of S

100 eductase inhibitor lovastatin on the Ewing's sarcoma cell line CHP-100.

101 A variant of the multidrug-resistant human sarcoma cell line Dx5 was derived by co-selection with d

102 Studies of the human myoblast-derived RD sarcoma cell line further demonstrated that TM4SF protei

103 CIC-DUX4 fusion containing the DUX4 CTD in a sarcoma cell line inhibit IFNgamma induction of ISGs.

104 variant with the alternative C-terminus in a sarcoma cell line not expressing the canonical C-termina

105 glioblastoma cell line TX3868 and the human sarcoma cell line OsA-CL carry hsrs containing amplified

106 rozygous 3-methylcholanthrene-induced murine sarcoma cell line to CTL immunoselection, selecting for

107 d the growth of a patient-derived clear cell sarcoma cell line whose oncogenic potential is driven by

108 CF7/AdrR and MES-SA/Dx5 (a human MDR uterine sarcoma cell line) compared with their non-MDR parental

109 ultures of live tumor cells (MCA205, a mouse sarcoma cell line), NK cells, DCs, and T cells was asses

110 maintaining Igf2 expression in the synovial sarcoma cell line, and the increased IGF2 synthesis prot

111 d COL11A2 genes are expressed in the Ewing's sarcoma cell line, CADO-ES1.

112 ificantly suppressed the growth of MCA205, a sarcoma cell line, even when treatment was delayed to 7

113 Furthermore, Dicer1 null cells from a sarcoma cell line, though depleted of miRNAs, are compet

114 Using a patient-derived sarcoma cell line, we developed a predictive platform fo

115 e but was meanwhile reclassified as an ewing sarcoma cell line.

116 arthritic cartilage as well as by a synovial sarcoma cell line.

117 t not in a comparator KIT+/PKCtheta- Ewing's sarcoma cell line.

118 nt manner, in the MDM2 amplified, SJSA human sarcoma cell line.

119 ected with 5 x 10(6) cells of the A673 human sarcoma cell line.

120 lines, and fusion transcript detection in a sarcoma cell line.

121 32 with IC50 = 12 pM against MES SA (uterine sarcoma) cell line and 2 pM against HEK 293T (human embr

122 ed with that in edited 3'-methylcholanthrene sarcoma cell lines (i.e., some unedited cell lines expre

123 Herein, we use Kras(G12D) x p53(-/-) sarcoma cell lines (KP sarcomas) that we and others have

124 Three different human Ewing's sarcoma cell lines (TC71, RD, and A4573) were found to e

125 e associated with resistance to MTX in human sarcoma cell lines and a rat hepatoma cell line.

126 he G401 rhabdoid tumor and HS-SY-II synovial sarcoma cell lines and had a high degradation selectivit

127 examined global tyrosine phosphorylation in sarcoma cell lines and human tumor samples.

128 of monoclonal antibody (MoAb) 8H9 to Ewing's sarcoma cell lines and normal hematopoietic cells was st

129 mmunoscreen cDNA libraries from two synovial sarcoma cell lines and normal testis, resulting in the i

130 Sarcoma cell lines and primary human sarcoma samples wer

131 effects of varied anti-angiogenic agents in sarcoma cell lines and tumor models.

132 ed beta-catenin and LGR5 expression in Ewing sarcoma cell lines and tumors and noted marked intra- an

133 mmunizing cell line, but also by independent sarcoma cell lines and untransformed myoblastoid cell li

134 nduced apoptosis, indicating that these bone sarcoma cell lines are dependent on Src activity for sur

135 that selectively inhibit the growth of Ewing sarcoma cell lines by inducing apoptosis.

136 in groups of unedited 3'-methylcholanthrene sarcoma cell lines compared with that in edited 3'-methy

137 he effects of dasatinib in 12 cultured human sarcoma cell lines derived from bone and soft tissue sar

138 been shown to inhibit the growth of Kaposi's sarcoma cell lines in vitro and in immunodeficient mice.

139 ne and in combination with rapamycin against sarcoma cell lines in vitro and xenograft models in vivo

140 ced expression of thrombospondins in Ewing's sarcoma cell lines inhibited the rate of tumor formation

141 ls, we have recently demonstrated that human sarcoma cell lines often inappropriately express high le

142 ASNS silencing in mouse and human sarcoma cell lines reduced the percentage of S phase cel

143 Rescue of BAF47 in BAF47-deficient sarcoma cell lines results in increased genome-wide BAF

144 interaction they identified in which Ewing's sarcoma cell lines showed an increased sensitivity to PA

145 Analysis of synovial sarcoma cell lines showed that either IGF-1R or the PDGF

146 All Ewing's sarcoma cell lines tested expressed Fas on their surface

147 tal human sarcoma cell line (2C4) as well as sarcoma cell lines that are deficient in JAK2 expression

148 describe an induction of apoptosis by p21 in sarcoma cell lines that is p53-independent and can be am

149 1 expression diminished the ability of Ewing sarcoma cell lines to proliferate and form colonies in s

150 ma, we generated stable DDX3-knockdown Ewing sarcoma cell lines using DDX3-specific small hairpin RNA

151 We first characterized 6 Ewing sarcoma cell lines using mRNA sequencing.

152 In addition, Ewing's sarcoma cell lines were able to serve as stimulators for

153 Moreover, treatment of Ewing sarcoma cell lines with PF-562271 induced apoptosis and

154 (HeLa, NIH3T3) and homologous cells (Ewing's sarcoma cell lines).

155 expressed on primary osteoblasts, osteogenic sarcoma cell lines, and primary fibroblasts.

156 In a set of sarcoma cell lines, immunoblotting confirmed nuclear loc

157 the most in vitro activity against Kaposi's sarcoma cell lines, was selected for the clinical invest

158 In a panel of seven Ewing's sarcoma cell lines, we found transactivation of a transi

159 Utilizing various sarcoma cell lines, xenografts and human tissue microarr

160 ctivity at nanomolar concentrations in these sarcoma cell lines.

161 BL6 murine melanoma and M5076 murine ovarian sarcoma cell lines.

162 class II-negative M12.C3 B lymphoma and Sal sarcoma cell lines.

163 short- and long-term rapamycin treatment in sarcoma cell lines.

164 EWS/FLI target genes across different Ewing sarcoma cell lines.

165 d but not wild-type bladder cancer and Ewing sarcoma cell lines.

166 served across multiple patient-derived Ewing sarcoma cell lines.

167 th and migration across a series of synovial sarcoma cell lines.

168 vels, and evaluated cytotoxicity of RK-33 in sarcoma cell lines.

169 es the level of the RRM2 protein in multiple sarcoma cell lines.

170 important functional role in pediatric Ewing sarcoma cell lines.

171 mpaired growth and colony formation in Ewing sarcoma cell lines.

172 yses, were performed using CRL-1976 and U2OS sarcoma cell lines.

173 t target gene in human tumor-derived Ewing's sarcoma cell lines.

174 WT1 expression and VEGF expression in Ewing sarcoma cell lines.

175 arked decrease in CASP3 transcripts in Ewing sarcoma cell lines.

176 In contrast, in the Ewing's sarcoma cells lovastatin triggered differentiation witho

177 ive tissue matrix from Engelbreth-Holm-Swarm sarcoma cells (Matrigel) modulated their phenotype: alka

178 Asparagine reliance of sarcoma cells may represent a metabolic vulnerability wi

179 Dystrophin inhibits myogenic sarcoma cell migration, invasion, anchorage independence

180 MCA205 (H2b) sarcoma cells mixed with either vIL-10-, mIL-10-, or Zeo

181 Mechanistically, hypoxia-induced PLOD2 in sarcoma cells modified COLVI, which was then secreted in

182 We observed that hypoxic gradients guide sarcoma cell motility and matrix remodeling through hypo

183 n amplifies PLOD2, which in turn accelerates sarcoma cell motility and metastasis.

184 In Ewing sarcoma cells, NOTCH signaling is abrogated by the drive

185 Culturing NELL1 knockout sarcoma cells on wild-type OS-enriched matricellular pro

186 o affected control kidney cell lines and the sarcoma cells; only podocytes are significantly less aff

187 o advanced bone cancer pain, osteolytic 2472 sarcoma cells or media were injected into the intramedul

188 ediated silencing of USP14 or UCHL5 in Ewing sarcoma cells produced significant growth inhibition.

189 Loss of TNC function in Ewing sarcoma cells profoundly inhibited their migratory and m

190 plays a major role in male fertility, Ewing sarcoma cell proliferation, and parathyroid cell functio

191 iral G protein-coupled receptor and Kaposi's sarcoma cell proliferation.

192 h chromatin remodeling complexes to regulate sarcoma cell proliferation.

193 ied the helicase CHD4 as essential for Ewing sarcoma cell proliferation.

194 eting of the molecular networks that support sarcoma cell proliferation.

195 oteasome as a node of vulnerability in Ewing sarcoma cells, providing orthologous confirmation of the

196 y, depletion of SYT-SSX2 in primary synovial sarcoma cells resulted in loss of nuclear beta-catenin s

197 cycline-inducible expression system in human sarcoma cells (SaOs-2) that lack both functional retinob

198 e dominant-negative form of CBP into Ewing's sarcoma cells sensitizes these cells against genotoxic o

199 USP6-expressing Ewing sarcoma cells stimulated migration of primary human mono

200 ating factors for recently established human sarcoma cell strains.

201 ts indicate that anchorage-independent Ewing sarcoma cells suppress anoikis through a pathway involvi

202 e loss of this regulatory mechanism promotes sarcoma cell survival and treatment resistance.

203 ers and super-enhancers, CHD4 promoted Ewing sarcoma cell survival not by modulating EWS-FLI1 activit

204 lective cytotoxicity of EA in human synovial sarcoma cells (SW982 cells) and investigated the mechani

205 e tumor cell lines including U2OS osteogenic sarcoma cells, SY5Y neuroblastoma cells, and MCF breast

206 In Ewing's sarcoma cells that express endogenous EWS/Fli-1, this li

207 Sarcoma cells that expressed exogenous ACTG2(R148S) inco

208 We show in human and murine synovial sarcoma cells that SS18-SSX increases BCL2 expression, b

209 mary melanocytes and melanoma and clear cell sarcoma cells through hypoxia inducible factor 1 (HIF1)-

210 ed genes and pro-inflammatory factors in the sarcoma cells, thus directing immune cell recruitment in

211 ous ETV6 but not EWS::FLI1 proteins in Ewing sarcoma cells, thus suppressing Ewing sarcoma growth.

212 EB1, GRHL2 gene regulatory network may drive sarcoma cells to a more epithelial-like state and that t

213 LIP expression significantly increased human sarcoma cells to both FasL-induced and tumor necrosis fa

214 ulted in an increased sensitivity of Ewing's sarcoma cells to chemotherapeutic agents, suggesting a r

215 tly increased the sensitivity of these human sarcoma cells to FasL- and TRAIL-induced apoptosis.

216 Exposure of Ewing's sarcoma cells to lactacystin resulted in accumulation of

217 y exposing 15 expanded populations of MES-SA sarcoma cells to paclitaxel (Taxol) at a concentration o

218 cal compounds for growth inhibition of Ewing sarcoma cells to provide the basis for the development o

219 maciclib was used first to prime Rb-positive sarcoma cells to reversibly arrest in G1 phase.

220 Additionally, d(GGAA)(3)s sensitized Ewing sarcoma cells to standard chemotherapy, suggesting their

221 s revealed a particular sensitivity of Ewing sarcoma cells to the inhibition of poly(ADP-ribose) poly

222 Here, using phospho-profiling, we find Ewing sarcoma cells treated with chemotherapeutic agents activ

223 olymerase chain reaction (RT-PCR) in Ewing's sarcoma cell tumour cell lines.

224 b inhibits migration and invasion of diverse sarcoma cell types and selectively blocks the survival o

225 atin conformation and transcription in Ewing sarcoma cells using a well-validated 'knock-down/rescue'

226 ulation of the proto-oncogene CCND1 in Ewing sarcoma cells via alternative complexes formed by DHX9 w

227 al and anchorage-independent growth in Ewing sarcoma cells via attenuating the accumulation of BNIP3L

228 LDH inhibitors affected Ewing sarcoma cell viability both in vitro and in vivo by redu

229 nscriptional activity significantly impaired sarcoma cell viability in vitro and in vivo.

230 entical target loci present in HT-1080 human sarcoma cells were all successfully corrected by gene ta

231 DDX3-knockdown and RK-33-treated Ewing sarcoma cells were compared with wild-type cells using a

232 Osteolytic sarcoma cells were implanted into the medullary space of

233 n in vivo model where murine osteolytic 2472 sarcoma cells were injected and confined to the intramed

234 DsRed2-labeled 2472 sarcoma cells were placed in Tg/NCD osteoclastogenic cul

235 Murine 2472 (2) sarcoma cells were transduced with fusion genes containi

236 6 mice produced NO-dependent cytotoxicity in sarcoma cells, whereas macrophages from NOS II-/- C57BL/

237 a potent cytotoxic effect on human synovial sarcoma cells which is mediated by heteromeric TRPC4/C1

238 (a) While NIH 3T3, mouse fibrosarcoma, and sarcoma cells, which respond to PLA2-I stimulation, expr

239 remodeling complex, specifically in synovial sarcoma cells, while sparing cardiomyocytes.

240 s capable of detecting contaminating Ewing's sarcoma cells with a sensitivity of one cell in 10(6) no

241 to tumor regression and replacement of Ewing sarcoma cells with benign fat cells.

242 Treatment of synovial sarcoma cells with dasatinib led to apoptosis and inhibi

243 Conversely, mitogenic stimulation of Ewing sarcoma cells with IGF1 impaired Sam68/DHX9 interaction

244 ed a phenotype that was reminiscent of Ewing sarcoma cells with partial EWS/ETS loss of function.

245 Sarcoma cells with upregulated IFN signaling that show h