ライフサイエンスコーパス: human cancer cell

1 er exogenous DNA damage and spontaneously in human cancer cells.

2 ption 3 (STAT3) and upregulated TGF-beta1 in human cancer cells.

3 with DNA-damaging and antimitotic agents on human cancer cells.

4 ools to study the properties of the BRCA1 in human cancer cells.

5 is critical in controlling p53 activities in human cancer cells.

6 he likelihood of observing an interaction in human cancer cells.

7 bilizing protein, at serine 16 in metastatic human cancer cells.

8 an interaction that we show is conserved in human cancer cells.

9 nt small interfering RNA delivery vehicle in human cancer cells.

10 omere maintenance functions of telomerase in human cancer cells.

11 ght therefore promote genetic alterations in human cancer cells.

12 ucing potential of a panel of fatty acids in human cancer cells.

13 nduced, but not oleate-induced, autophagy in human cancer cells.

14 growth of a xenotransplant of MYC-amplified human cancer cells.

15 on, whereas miR-141 suppresses malignancy in human cancer cells.

16 or high MYC protein levels in 8q24-amplified human cancer cells.

17 th factor (EGF)-stimulated cells and diverse human cancer cells.

18 erone HSP90 binds to and stabilizes PRKD2 in human cancer cells.

19 ed the oncolytic potency of these viruses on human cancer cells.

20 CND1, D3 and G1 and for the proliferation of human cancer cells.

21 tes that these effects are not restricted to human cancer cells.

22 raps for NF-Y and thus inhibit the growth of human cancer cells.

23 e in antiproliferative assays using cultured human cancer cells.

24 tion of growth and induction of apoptosis in human cancer cells.

25 bitors induces robust apoptosis in different human cancer cells.

26 than G-quadruplex sequence, in chromosome of human cancer cells.

27 that potently inhibit the growth of cultured human cancer cells.

28 A replication through Lyn phosphorylation in human cancer cells.

29 s chalcone derivatives inhibit the growth of human cancer cells.

30 deliver peptides to intracellular targets in human cancer cells.

31 natural genetic and epigenetic diversity of human cancer cells.

32 e can support the growth of various types of human cancer cells.

33 of calcitonin and each of its precursors in human cancer cells.

34 ring resistance to cisplatin and olaparib in human cancer cells.

35 (EGFR) and the Hippo pathway effector TAZ in human cancer cells.

36 nzyme poisoning activity and cytotoxicity to human cancer cells.

37 apoptosis, and inhibits the proliferation of human cancer cells.

38 activated rapidly within only hNQO1-positive human cancer cells; addition of an hNQO1 inhibitor preve

39 be adapted to study the interactions between human cancer cells and a humanized bone microenvironment

40 icromolar antiproliferative activity towards human cancer cells and are active in vivo.

41 r, Y26 phosphorylation of PGAM1 is common in human cancer cells and contributes to regulation of 3-ph

42 Using H929 human cancer cells and drosophila S2R+ cells, our data r

43 By studying these variants in human cancer cells and Drosophila, we uncovered that MOB

44 al significance, we overexpressed miR-335 in human cancer cells and found that it caused growth suppr

45 ine 15 to activate the cell death program in human cancer cells and in murine B cells.

46 Here, the application of PINEM on whole human cancer cells and membrane vesicles isolated from t

47 or with a broad anticancer effect in various human cancer cells and mouse models of breast cancer.

48 Here, using human cancer cells and patient-derived xenografts in mic

49 n in EGF-stimulated cells as well as diverse human cancer cells and primary leukemia cells from human

50 hosphorylation of PDP1 was common in diverse human cancer cells and primary leukemia cells from patie

51 egulated across multiple types of aggressive human cancer cells and primary tumors.

52 However, the interplay between the implanted human cancer cells and recruited mouse stromal and immun

53 Moreover, DDX24 is overexpressed in human cancer cells and reduction of DDX24 protein levels

54 the acetylation levels of endogenous p53 in human cancer cells and subsequently promotes p53-mediate

55 s a hypoxia-inducible, VHL-regulated gene in human cancer cells and that expression of IL11 mRNA was

56 Nonresistant human cancer cells and their multidrug resistant variant

57 monomeric analogues for binding to different human cancer cells and tissues.

58 onal groups, inhibits the growth of cultured human cancer cells at nanomolar-picomolar concentrations

59 Human cancer cells bear complex chromosome rearrangement

60 Human cancer cells (breast MCF7, breast-to-lung metastat

61 rmin to mice inhibited the growth of control human cancer cells but not those expressing NDI1.

62 down-regulation alters cell proliferation in human cancer cells by inducing both apoptosis and cell c

63 mmonly activated in EGF-stimulated cells and human cancer cells by lysine acetylation.

64 ly dividing cells, including the majority of human cancers, cells bypass this growth limit through te

65 Impaired DDR in SALL4-deficient human cancer cells can be rescued by the restored expres

66 It is, however, unclear whether human cancer cells can be similarly reprogrammed and sub

67 rome fibroblasts or by depletion of BLM from human cancer cells confirms a role for Sgs1/BLM in suppr

68 tory activities and potent cytotoxicities in human cancer cell cultures and reduced lethality in an a

69 e inhibitory data and cytotoxicity data from human cancer cell cultures establish that modification o

70 e inhibitory data and cytotoxicity data from human cancer cell cultures were used to establish struct

71 Compounds 16b and 17b are the most potent in human cancer cell cultures with MGM GI50 values of 0.063

72 0) values of 21-71 nM in the NCI panel of 60 human cancer cell cultures.

73 sized were also evaluated against a panel of human cancer cells demonstrating a promising antitumoral

74 In human cancer cells, driver reactions play pivotal roles

75 hows promising antiproliferative activity on human cancer cells, endorsing their further exploration

76 Here, we show that genetically distinct human cancer cells exploit eIF4E2-directed protein synth

77 Additionally, we found that human cancer cells expressed a functional IL-11Ra subuni

78 eficient and -proficient Chinese hamster and human cancer cells for synthetic lethality application u

79 eless showed a greater level of infection of human cancer cells (glioma and melanoma) than of normal

80 inding, and offer control of toxicity toward human cancer cells, Gram positive and negative bacteria,

81 s that can positively or negatively regulate human cancer cell growth.

82 dated SF3B1 as a CYCLOPS gene and found that human cancer cells harboring partial SF3B1 copy-loss lac

83 ingly suppresses the growth of both, fly and human cancer cells harbouring oncogenic Ras mutations.

84 ssed in Fbxo4 knockout cells, tissues and in human cancer cells, harbouring inactivating Fbxo4 mutati

85 6]-shogaol had measurable activities against human cancer cells HCT-116 and H-1299.

86 man DEAD-box RNA helicases in two permissive human cancer cells (HeLa and A549), one semi-permissive

87 acoustic waves (SAW) to differentially lyse human cancer cells in a chemical-free manner.

88 establishment, progression and metastasis of human cancer cells in athymic mice.

89 lular and extracellular levels of lactate in human cancer cells in vitro and in melanoma tumors ex vi

90 r DNA quadruplexes and inhibit the growth of human cancer cells in vitro and in vivo.

91 a drug delivery platform via co-culture with human cancer cells in vitro.

92 rms various sizes of cytoplasmic clusters in human cancer cells, independent of protein expression le

93 sed proliferation and increased apoptosis in human cancer cells, indicating that STAT3 is a viable mo

94 abundance correlated with MPE formation in a human cancer cell-induced effusion model.

95 Xenograft tumors grown from human cancer cells injected with v6 peptides were smalle

96 Orthotopic or systemic inoculation of tagged human cancer cells into the mouse leads to the release o

97 astasis to the bone rely on the injection of human cancer cells into the mouse skeleton.

98 for determining the tumorigenic potential of human cancer cells is a xenotransplantation into immunod

99 MYXV tropism for human cancer cells is largely mediated by intracellular

100 ntrolled expression induces rereplication in human cancer cells, is upregulated in E7-expressing cell

101 is commonly activated in diverse metastatic human cancer cells, leading to up-regulation of a CREB t

102 It is clear, however, that loss of BRCA1 in human cancer cells leads to chromosomal instability (CIN

103 Cytoplasmic retention of IMP-3 and HNRNPM in human cancer cells leads to significant drop in prolifer

104 that activation of NRF2, in either mouse or human cancer cells, leads to increased dependency on exo

105 The same relationship is observed in a human cancer cell line (K562), and we postulate that fou

106 sample derived from the HPV type 16 positive human cancer cell line (SiHa), and failed to detect the

107 ndonuclease-induced DSBs near telomeres in a human cancer cell line are much more likely to generate

108 itro models employ primary rodent neurons or human cancer cell line cells in low throughput formats.

109 -induced translation stress, and analysis of human cancer cell line data from Project Achilles furthe

110 e use in cancer therapy.For our analysis the human cancer cell line H441 (a human lung adenocarcinoma

111 lice variants as the transgenic mice and the human cancer cell line MDA-MB 321.

112 transplantable metastasis model derived from human cancer cell line MDA-MB-231.

113 Experiments involving a human cancer cell line panel and mouse xenografts reveal

114 Metabolic profiling of human cancer cell line revealed that TAp73 activates ser

115 ting RNA-seq with p53 ChIP-seq analyses of a human cancer cell line under DNA damage, we define a hig

116 DKK1 to CKAP4, suppressed AKT activity in a human cancer cell line, and attenuated xenograft tumor f

117 BQS is severely compromised in a human cancer cell line, suggesting that loss of BQS migh

118 required for proliferation and survival in a human cancer cell line.

119 Antiproliferative activity in three human cancer cell lines (A549, CH1, SW480) was determine

120 xicity of the compounds was studied in three human cancer cell lines (CH1, SW480, and A549) by means

121 ntiproliferative activity against a panel of human cancer cell lines (including cisplatin and multidr

122 ased on the measured growth inhibition of 60 human cancer cell lines (NCI60) in the presence of fulve

123 y but enhanced cytotoxic effects against the human cancer cell lines A2780, Cal27, Kyse510, and MDA-M

124 Myristica species was evaluated against five human cancer cell lines A549, DLD-1, DU145, FaDu and MCF

125 A survey of human cancer cell lines also show a similar wide variati

126 pool and evaluated against a panel of three human cancer cell lines and a normal cell line.

127 glycopeptides from 250 proteins across three human cancer cell lines and also discovered unexpected p

128 hat K-Ras4A was widely expressed in 30 of 30 human cancer cell lines and amounts equal to K-Ras4B in

129 hibited antitumor activities against several human cancer cell lines and appeared to arrest cell cycl

130 We apply the method to human cancer cell lines and biopsied cancer tissue, ther

131 ound that it was broadly upregulated in many human cancer cell lines and cancers, including most nota

132 trated for quantitative miR-107 detection in human cancer cell lines and clinical urine samples.

133 n be mapped onto 1,001 molecularly annotated human cancer cell lines and correlated with sensitivity

134 We examined BCLb mRNA in a panel of human cancer cell lines and did not observe the extensiv

135 re (autologous and allogeneic) with multiple human cancer cell lines and dissociated primary cancer s

136 pounds, which were tested against aggressive human cancer cell lines and for protein synthesis inhibi

137 Ai data derived from screening more than 100 human cancer cell lines and identified HNF1B as a transf

138 itotic entosis occurs constitutively in some human cancer cell lines and mitotic index correlates wit

139 Finally, our data generated from both human cancer cell lines and mouse xenograft model showed

140 apy-resistant high-mesenchymal cell state in human cancer cell lines and organoids and show that it d

141 he cytotoxic effects of ARGX-111 in multiple human cancer cell lines and patient-derived primary tumo

142 e further supported by consistent results in human cancer cell lines and primary samples of human hae

143 djacent host genomic structural variation in human cancer cell lines and primary tumors.

144 is combined with HSP90 inhibition in various human cancer cell lines and tumor models.

145 ese antibodies bind hypoglycosylated MUC1 on human cancer cell lines and tumor tissues but show no re

146 However, mice do not have the IL-8 gene, so human cancer cell lines and xenograft studies have been

147 known (-)-agelastatin alkaloids against nine human cancer cell lines are described.

148 their characteristics of binding to various human cancer cell lines as well as to primary human leuk

149 potent anti-proliferative activities against human cancer cell lines by inhibiting tubulin polymeriza

150 ies at subnanomolar concentration against 60 human cancer cell lines conducted by Developmental Thera

151 of a diverse chemical library in a panel of human cancer cell lines cultured under different growth

152 ultures of mouse primary tumor spheroids and human cancer cell lines displayed increased cell prolife

153 isplayed potent cytotoxicity against several human cancer cell lines due to tubulin inhibition, as sh

154 In vitro analysis of STAT3 in human cancer cell lines has elucidated a number of speci

155 were also shown to inhibit migration of two human cancer cell lines in monolayer scratch assays.

156 ehydrogenase(bright)) from a wide variety of human cancer cell lines in vitro and dissociated primary

157 vel agents was established in wide ranges of human cancer cell lines in vitro and in vivo in rodents.

158 moderate to potent activities against three human cancer cell lines in vitro.

159 vation and cell growth inhibition in several human cancer cell lines including H460 and HCT116(+/+) c

160 NEAT1 targeting in established human cancer cell lines induced synthetic lethality with

161 these cyclins in a significant manner in six human cancer cell lines of different origins.

162 inhibited the growth of multiple RAS-mutant human cancer cell lines of diverse tissue origin by bloc

163 Expression of the designed inhibitors in human cancer cell lines revealed unique dependencies on

164 Biological investigation of 2-5 on human cancer cell lines showed enhancement of antiprolif

165 nducted with 2-anthrol derivative 7 on three human cancer cell lines showed higher activity for irrad

166 Analyzing a panel of human cancer cell lines spanning a wide range of express

167 In all human cancer cell lines studied, the 90-kDa wild-type RS

168 Our results for several human cancer cell lines suggest that interfacial geometr

169 st of them are more cytotoxic to a number of human cancer cell lines than cisplatin.

170 soluble 2) are more cytotoxic to a number of human cancer cell lines than cisplatin.

171 splays greater potency against a spectrum of human cancer cell lines than current OV candidates.

172 using the NCI-H460 lung and A431 epidermoid human cancer cell lines that EGFR binding to anterior gr

173 together with recently reported evidence in human cancer cell lines that ETAA1 activates ATR kinase

174 , enabled formation of extensive syncytia by human cancer cell lines that express the target receptor

175 Across 643 human cancer cell lines that were analyzed, elevated AXL

176 n vitro cytotoxicity evaluation against four human cancer cell lines THP-1 (leukemia), A-549 (lung),

177 We screened a panel of over 600 human cancer cell lines to identify markers of resistanc

178 By comparing PG-G hydrolysis across human cancer cell lines to serine hydrolase activities d

179 sed a genome-scale shRNA viability screen in human cancer cell lines to systematically identify genes

180 Antiproliferative activity in four human cancer cell lines was determined by MTT assay, yie

181 ity of synthetic haliclamide against several human cancer cell lines was found to be in the high muM

182 Using diverse human cancer cell lines we show that this occurs only in

183 idely used classes of antineoplastic agents, human cancer cell lines were treated with the Akt inhibi

184 at forced expression of a second oncogene in human cancer cell lines with an endogenous mutated oncog

185 The agent selectively kills human cancer cell lines with high HDAC and CTSL activiti

186 nalogues show cytotoxicity against different human cancer cell lines with IC50 values between 16.4 an

187 mal mouse intestinal epithelia and adenomas, human cancer cell lines with or without drug treatments,

188 Depletion of RBPJ in human cancer cell lines xenografted into immunodeficient

189 )P HotSpot assay) and in vivo (IC50 < 2 muM, human cancer cell lines) ACK1 inhibition.

190 In a panel of nine human cancer cell lines, all compounds were either sligh

191 S3L2 overexpression suppressed the growth of human cancer cell lines, and knockdown enhanced the grow

192 and underexpressed in a large percentage of human cancer cell lines, and primary human lung cancer s

193 n, and sonicated fibrils in two immortalised human cancer cell lines, Caco-2 and Hec-1a.

194 utant allelic imbalance was also observed in human cancer cell lines, consistent with a requirement f

195 lay modest cytotoxicity toward seven diverse human cancer cell lines, exhibiting IC(50) values rangin

196 itro antitumor properties against a panel of human cancer cell lines, including cisplatin- and multid

197 otic activity when tested against a panel of human cancer cell lines, including cisplatin-resistant c

198 H were readily taken up by two wild types of human cancer cell lines, MCF-7 breast adenocarcinoma and

199 IHSF115 is cytotoxic for a variety of human cancer cell lines, multiple myeloma lines consiste

200 xamined for their cytotoxicity on a panel of human cancer cell lines, their cardioprotection against

201 By profiling the response of over 120 human cancer cell lines, we derived an expression-based

202 the most cytotoxic complexes against various human cancer cell lines, with a potency similar to that

203 to study genome-wide chromatin structure in human cancer cell lines, yet numerous technical challeng

204 Furthermore, Arf1 inhibitors reduced CSCs in human cancer cell lines.

205 ated for their cytotoxicity against selected human cancer cell lines.

206 relationships were investigated using three human cancer cell lines.

207 ts loss impairs the proliferation of several human cancer cell lines.

208 at citral inhibits proliferation of multiple human cancer cell lines.

209 ough hallmarks of DNA damage are detected in human cancer cell lines.

210 apply it for KRAS mutation analysis of four human cancer cell lines.

211 eletion, inhibits cell growth in RB-negative human cancer cell lines.

212 ide polymorphism (SNP) array analysis of 675 human cancer cell lines.

213 through in vivo selection from heterogeneous human cancer cell lines.

214 tiproliferative activities against different human cancer cell lines.

215 possessing a strong antimitotic activity in human cancer cell lines.

216 arkable anticancer activity against multiple human cancer cell lines.

217 tificial liposomes and cytotoxic activity on human cancer cell lines.

218 ntext of a large dataset of drug response in human cancer cell lines.

219 depletion of GGPP, in a variety of different human cancer cell lines.

220 roblasts and anchorage-independent growth of human cancer cell lines.

221 , A549, MCF-7, TSGH, MKN45, HT29, and HCT116 human cancer cell lines.

222 c-Met in prostate tumor progenitor cells and human cancer cell lines.

223 ts downstream signaling cascades in multiple human cancer cell lines.

224 ts from large-scale chemical screening using human cancer cell lines.

225 s and protein isoprenylcysteines by cultured human cancer cell lines.

226 ative effect was monitored on four different human cancer cell lines.

227 f approximately 1300 single drugs on several human cancer cell lines.

228 e cancers and androgen regulated in cultured human cancer cell lines.

229 )-pseudotyped retroviruses poorly entered 53 human cancer cell lines.

230 d in prostate, colon and bladder tumors, and human cancer cell lines.

231 thelial growth factor (VEGF) in a variety of human cancer cell lines.

232 oncentrations to cultures of three different human cancer cell lines.

233 ng somatic development in mice as well as in human cancer cell lines.

234 uM against Hep3B, MDA-MB-231, PC-3, and A549 human cancer cell lines.

235 termined at a ratio 1:6 (named PRP) using 24 human cancer cell lines.

236 oss-of-function screens performed in diverse human cancer cell lines.

237 ity and invasiveness of the SW480 and Hs578T human cancer cell lines.

238 We also measured expression by 15 human cancer cell lines.

239 with GI50 values below 10 nM in a variety of human cancer cell lines.

240 al and polar fractions was evaluated on nine human cancer cell lines.

241 w low nanomolar cytotoxicity toward multiple human cancer cell lines.

242 and enrich a large number of MTs (>50) from human cancer cell lysates with remarkable specificity ov

243 impressive activities against drug resistant human cancer cells, making them desirable for potential

244 In this study, we report that in human cancer cells, metformin inhibits mitochondrial com

245 We have discovered that in human cancer cells (myeloma, lymphoblastoid, and breast

246 in the presence of an up-regulated enzyme in human cancer cells, NAD(P)H: quinone oxidoreductase-1 (N

247 e assessed: (a) inhibition of cell growth of human cancer cells (NCI), (b) induction of morphological

248 When exposed to human cancer cells, NK cell expanded ex vivo in the pres

249 ligands of Siglec-7 and -9 were expressed on human cancer cells of different histological types.

250 ti-EpCAM antibody that specifically binds to human cancer cells of epithelial origin such as pancreat

251 proteasome-mediated degradation of STK33 in human cancer cells of various tissue origin in vitro and

252 egradation of PRKD2, augmenting apoptosis in human cancer cells of various tissue origins.

253 Depletion of MCM8 or MCM9 in human cancer cells or the loss of function MCM9 mutation

254 uption of endogenous BubR1.Bub3 complexes in human cancer cells phenocopies the effects observed in g

255 Through in vivo selection of human cancer cell populations, we uncover a convergent a

256 We found that different mouse and human cancer cells produced greater levels of p40 than p

257 cascade in eukaryotes, and in inhibition of human cancer cell proliferation.

258 vertebrate embryonic neural development and human cancer cell proliferation.

259 Here we show that human cancer cells rapidly use exogenous serine and that

260 ee example separations: live and dead yeast; human cancer cells/red blood cells; and rodent fibroblas

261 dy, we show that overexpression of miR-96 in human cancer cells reduces the levels of RAD51 and REV1

262 Knockdown of A2BR on mouse and human cancer cells reduces their metastasis in vivo and

263 ation of Plasmodium falciparum parasites and human cancer cells require de novo pyrimidine synthesis

264 ctions is one of the most common features of human cancer cells, restoring p53 expression and activit

265 knockdown or LDHA Y10F rescue expression in human cancer cells resulted in decreased tumour metastas

266 Moreover, in murine tissues and human cancer cells, RIP140 stimulated APC transcription

267 Reducing PASD1 in human cancer cells significantly increases the amplitude

268 The upregulation of HP1alpha in human cancer cells suppressed open chromatin, glycolysis

269 and suppressing malignant transformation in human cancer cells that depend on STAT3.

270 ke of functionalized gallium corroles by all human cancer cells that followed the order: 4 >> 3 > 2 >

271 or partially permissive for the majority of human cancer cells that harbor defects in antiviral sign

272 equired for maintaining low levels of p53 in human cancer cells that harbor mutant K-Ras and wild-typ

273 Herein we show in a diverse array of human cancer cells that IMP2 overexpression stimulates a

274 mparison of cell surface-exposed proteins in human cancer cells that were tightly synchronized in mit

275 Furthermore, TLS affords human cancer cells the ability to counteract chemotherap

276 ion of novel variation in microorganisms and human cancer cells, the extent to which the natural envi

277 idant and antiproliferative activity against human cancer cells through apoptosis; nuclear apoptosis

278 FOXM1 and HSP70 increases the sensitivity of human cancer cells to anticancer drug-induced apoptosis.

279 The acquired resistance of human cancer cells to apoptosis is one of the defining h

280 Furthermore, PI-1840 sensitizes human cancer cells to the mdm2/p53 disruptor, nutlin, an

281 onitored NF-kappaB and caspase signalling in human cancer cells treated with a short pulse of Tumour

282 Human cancer cells treated with CFI-402257 exhibit effec

283 l transition (EMT) markers were performed on human cancer cells treated with PRP.

284 In human cancer cells, tTG activates signaling pathways tha

285 ave been prepared, and cell viability of two human cancer cell types (breast and glioblastoma) was de

286 Here, constricted migration of two human cancer cell types and primary mesenchymal stem cel

287 However, there is no direct evidence that human cancer cells undergo an EMT.

288 In human cancer cells, we found that changes in the maximum

289 fy host factors relevant for MYXV tropism in human cancer cells, we performed a small interfering RNA

290 Luciferase-tagged CRC cell lines and human cancer cells were injected intrarectally into nono

291 blocks apoptosis and drives proliferation in human cancer cells where it is commonly elevated.

292 ed in cells stimulated by EGF and in diverse human cancer cells, where ACAT1 tetramers, but not monom

293 regulate CHCM1/CHCHD6 expression in multiple human cancer cells, whereas mitochondrial respiratory ch

294 dependent growth, migration, and invasion of human cancer cells, which depend on STAT3.

295 ctive agent, 2j, showed high potency against human cancer cells with IC50s ranging from 0.05 to 1.7 m

296 and markedly suppressed the proliferation of human cancer cells with less cytotoxic effects against n

297 Treatment of human cancer cells with S3I-1757 (but not a closely rela

298 n of several HSP90 clients upon treatment of human cancer cells with the clinical HSP90 inhibitor 17-

299 Treatment of human cancer cells with these nanoparticles in vitro tri

300 etion markedly reduces the tumorigenicity of human cancer cell xenografts in mice.