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

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

4 rogate the cytotoxic effects of cisplatin on human cancer cells.

5 natural genetic and epigenetic diversity of human cancer cells.

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

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

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

9 nzyme poisoning activity and cytotoxicity to human cancer cells.

10 stem in regulating the migration of amoeboid human cancer cells.

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

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

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

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

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

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

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

18 tural studies of p53 assemblies derived from human cancer cells.

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

20 omere maintenance functions of telomerase in human cancer cells.

21 crease in aneuploidy in checkpoint-deficient human cancer cells.

22 ght therefore promote genetic alterations in human cancer cells.

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

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

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

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

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

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

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

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

31 lex structures and increase R loop levels in human cancer cells.

32 ty to trigger DNA damage in rapidly dividing human cancer cells.

33 LRPPRC acted as an inhibitor of autophagy in human cancer cells.

34 ave demonstrated a dual targeting of GLS2 in human cancer cells.

35 sly increase R-loop levels within minutes in human cancer cells.

36 unconventionality in TERT expression across human cancer cells.

37 al activation of WNT by AP-1 is conserved in human cancer cells.

38 WRN function induces cellular senescence in human cancer cells.

39 ying) in culture without general toxicity to human cancer cells.

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

41 d antiproliferative activity toward cultured human cancer cells, a favorable in vivo pharmacokinetic

42 In cocultures with primary human cancer cells, actively migrating monocyte-derived

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

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

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

46 completely inhibited ADO production in both human cancer cells and CD8(+) T cells.

47 ybrid nucleosomes that are known to exist in human cancer cells and contain H3 histone variants CENP-

48 orylation can also be found in ERK-activated human cancer cells and contribute to tumorigenesis.

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

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

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

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

53 or-type kappa (PTPRK), as a Wnt inhibitor in human cancer cells and in the Spemann organizer of Xenop

54 Importantly, PTEN null human cancer cells and in vivo murine models are sensiti

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

56 analyze cell cycles in deep lineage trees of human cancer cells and mouse embryonic stem cells and de

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

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

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

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

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

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

63 ormally, Siglec-15 is broadly upregulated on human cancer cells and tumor-infiltrating myeloid cells,

64 FGL1 is highly produced by human cancer cells, and elevated FGL1 in the plasma of c

65 Human cancer cells bear complex chromosome rearrangement

66 Here, we report that, in human cancer cells, BRD4S forms nuclear puncta that poss

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

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

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

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

71 e degradation of stalled RFs in KB2P1.21 and human cancer cells by recruiting the base excision repai

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

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

74 Acute knockdown of DHX33 in multiple human cancer cells caused decreased Bcl-2 protein level,

75 r differences in DeltaPsim in unsynchronized human cancer cells, cells synchronized in G1, S, and G2,

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

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

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

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

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

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

82 In human cancer cells, depletion of miR181ab1 impaired prol

83 In human cancer cells, driver reactions play pivotal roles

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

85 eports showed that the knockdown of RBM10 in human cancer cells enhances the growth of mouse tumor xe

86 In both C. elegans and human cancer cells, ether-lipid synthesis protects again

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

88 DNA damage, and apoptosis were increased in human cancer cells following depletion of the B-family D

89 ocompromised zebrafish that robustly engraft human cancer cells for in excess of 28 d.

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

91 uch as nucleotides and are indispensable for human cancer cell growth.

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

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

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

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

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

97 s an inhibitor of UV photoproduct removal in human cancer cells in vitro via its ability to promote t

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

99 ct to induce high cytotoxicity in a range of human cancer cells, including T98g (glioma multiforme),

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

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

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

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

104 small laparotomy and direct implantation of human cancer cells into the bladder lumen.

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

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

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

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

109 Whereas this complex was highly cytotoxic in human cancer cells, it showed low toxicity in hemolysis

110 exhibits cytotoxic activity against various human cancer cells, killing SW48 colon cancer cells in p

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

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

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

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

115 The study was performed in a human cancer cell line (MCF7) and in mouse, non-cancerou

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

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

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

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

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

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

122 ns in uracil pattern upon drug treatments in human cancer cell line models derived from HCT116.

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

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

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

126 ine synthesis, and inhibited tumor growth in human cancer cell line xenografts.

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

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

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

130 d HOXA-AS2 and the miR-126-3p, in a panel of human cancer cell lines (HCC, renal and breast carcinoma

131 tumour spheroids formed from two established human cancer cell lines (HCT116 and CAL27) to single and

132 p53 for proteasomal degradation in multiple human cancer cell lines (HCT116 and U2OS).

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

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

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

136 Exome sequences of 1,001 human cancer cell lines and 577 xenografts revealed most

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

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

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

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

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

142 we evaluated the toxicity of monensin in 24 human cancer cell lines and classified them as resistant

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

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

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

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

147 which has promising activity against several human cancer cell lines and inhibits tumor cell migratio

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

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

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

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

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

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

154 Gene expression profiling of 165 pairs of human cancer cell lines and their Cas9-expressing deriva

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

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

157 Human cancer cell lines are frequently used as model sys

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

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

160 s showed improved activity against mouse and human cancer cell lines defective in O-linked glycosylat

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

162 rmed genome-scale CRISPR-Cas9 screens in 324 human cancer cell lines from 30 cancer types and develop

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

164 Multifaceted characterizations of human cancer cell lines hold huge treasures for cancer r

165 HepG2 is one of the most widely used human cancer cell lines in biomedical research and one o

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

167 e of determining the metastatic potential of human cancer cell lines in mouse xenografts at scale.

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

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

170 e significant amount of PTX, killing several human cancer cell lines in vitro with a long lasting act

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

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

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

174 Gboxin toxicity extends to established human cancer cell lines of diverse organ origin, and sho

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

176 The new compounds were screened in the 60 human cancer cell lines of the NCI drug screen and showe

177 gainst A549, DU 145, HeLa, HCT 116, and MCF7 human cancer cell lines provide insights into the impact

178 ity assays against a representative panel of human cancer cell lines revealed that polyamines L1a and

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

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

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

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

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

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

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

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

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

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

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

190 On average, the sensitivity of human cancer cell lines to DNMDP is correlated with PDE3

191 s, we utilized RNA-sequencing data from 1011 human cancer cell lines to functionally link 8354 fusion

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

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

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

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

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

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

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

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

200 s of E3 ligase components across hundreds of human cancer cell lines(3-5), we identify CR8-a cyclin-d

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

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

203 these observations, Akt3 up-regulates p53 in human cancer cell lines, and the expression of Akt3 posi

204 25-fold increased cytotoxicity against five human cancer cell lines, and up to 70-fold less toxicity

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

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

207 In multiple human cancer cell lines, DHX33 was found to stimulate th

208 growth inhibitory activities against various human cancer cell lines, including A549, Caco-2, and SF2

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

210 death-ligand 1 expression in a wide range of human cancer cell lines, offering a route to decoupling

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

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

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

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

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

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

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

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

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

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

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

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

223 nd evaluation of their activity against five human cancer cell lines.

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

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

226 relationships were investigated using three human cancer cell lines.

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

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

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

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

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

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

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

234 tiproliferative activities against different human cancer cell lines.

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

236 arkable anticancer activity against multiple human cancer cell lines.

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

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

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

240 cytotoxic and target-mediated selectivity on human cancer cell lines.

241 ts proliferation, migration, and invasion in human cancer cell lines.

242 itochondrial membrane dissipation by DOX, in human cancer cell lines.

243 and celery that inhibits growth of fungi and human cancer cell lines.

244 I and eight complex derivatives against five human cancer cell lines.

245 eir biological evaluation against aggressive human cancer cell lines.

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

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

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

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

250 rtly after the discovery of RAS mutations in human cancer cells nearly 40 years ago.

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

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

253 r the acquisition of metabolic profiles from human cancer cells of variable origin.

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

255 inhibitor and show that CD80 is expressed by human cancer cells originating from both solid epithelia

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

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

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

259 ve G-quadruplex ligand that, when studied in human cancer cells, proved to be able to stabilize both

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

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

262 ion in the lal(-/-) lymph nodes and improves human cancer cell rejection.

263 on in lal(-/-) Tregs and Bregs, and improves human cancer cell rejection.

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

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

266 Moreover, human cancer cells show increased Win isoform expression

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 ession cloning approach to identify genes in human cancer cells that are able to complement the loss

270 e1 O-glycan T-antigen is a common feature of human cancer cells that correlates with metastasis.

271 nt findings (Tsabar et al.) demonstrate that human cancer cells that evade the cell cycle blockage no

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

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

274 In human cancer cells that harbor mutant KRAS and WT p53 (p

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

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

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

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

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

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

281 rms and performed experiments with suspended human cancer cells to characterize the performance of th

282 formed a targeted kinase inhibitor screen in human cancer cells to identify novel Hippo pathway regul

283 ining DNA repair pathway and hypersensitises human cancer cells to IR.

284 Using Drosophila neuroblasts and human cancer cells to study mitotic spindle assembly in

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

286 ell, an interpretable deep learning model of human cancer cells trained on the responses of 1,235 tum

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

288 Human cancer cells treated with CFI-402257 exhibit effec

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

290 In human cancer cells, tTG activates signaling pathways tha

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

292 Conversely, silencing NDRG1 in multiple human cancer cell types decreased MIG6 expression, demon

293 We demonstrate these observations in human cancer cells using mutational studies and identifi

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

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

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

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

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

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

300 ompound 1 was active against the tested five human cancer cells, with half maximal inhibitory concent