ライフサイエンスコーパス: HCT116 cell

1 h of 11 known components of cohesin in human HCT116 cells.

2 d the growth suppressive effects of MDFIC in HCT116 cells.

3 chromatin structure at this region by p53 in HCT116 cells.

4 candidate oxidoreductases were expressed in HCT116 cells.

5 iate HuR target mRNAs in Chk2-null (CHK2-/-) HCT116 cells.

6 ation of STAT3 by epidermal growth factor in HCT116 cells.

7 p53-dependent, more dramatically in TK6 than HCT116 cells.

8 ent in the KRAS mutant lines LS180, LoVo and HCT116 cells.

9 mary human foreskin keratinocytes (HFKs) and HCT116 cells.

10 ome instability of spontaneous polyploids in HCT116 cells.

11 did not alter the expression of Bcl-w RNA in HCT116 cells.

12 *NO-induced apoptosis of human colon cancer HCT116 cells.

13 uciferase transcription when introduced into HCT116 cells.

14 y which the kinase inhibitor lapatinib kills HCT116 cells.

15 ed kinases 1/2, and AKT, and radiosensitized HCT116 cells.

16 nhibited by exogenous mutant p53 in p53-null HCT116 cells.

17 ated LPA-mediated proliferation of SW480 and HCT116 cells.

18 ncreased NOS2 mRNA and protein expression in HCT116 cells.

19 3+/- and p53-/- isogenic clones derived from HCT116 cells.

20 -damaging and non-DNA-damaging conditions in HCT116 cells.

21 ntent observed after 4 h of DCA treatment of HCT116 cells.

22 ) were assessed using human colonic HT29 and HCT116 cells.

23 was generated by the disruption of DNMT1 in HCT116 cells.

24 es not interact with VDAC-2 in Bax-deficient HCT116 cells.

25 RNAi abolished LPA-induced proliferation of HCT116 cells.

26 whereas only KW2152 yielded sensitization in HCT116 cells.

27 orporated FU:Gua in the DNA of MMR-deficient HCT116 cells.

28 independent mechanisms in human colon cancer HCT116 cells.

29 ated in p53-positive but not in p53 knockout HCT116 cells.

30 n of hMLH1 alone can elevate MMR activity in HCT116 cells.

31 RK signaling and integrin alpha2 function in HCT116 cells.

32 ession of p53 and p21(Cip1) in wild-type p53 HCT116 cells.

33 nes, prevented butyrate-induced apoptosis in HCT116 cells.

34 /M arrest by SFN compared with the wild type HCT116 cells.

35 optosis induced by THG in human colon cancer HCT116 cells.

36 CT116 (p53+/+) cells but not in the p53-null HCT116 cells.

37 M1/2(-/-) knockouts in HEK293 and colorectal HCT116 cells.

38 ession in both Bax-proficient and -deficient HCT116 cells.

39 ed with the cyclin B1 promoter in irradiated HCT116 cells.

40 ed ERK, and slows the growth in soft agar of HCT116 cells.

41 tions are induced by oxaliplatin in parental HCT116 cells.

42 increase p21 protein levels in p53-deficient HCT116 cells.

43 Skp2 in cells, and reduced the viability of HCT116 cells.

44 repression and induced growth inhibition in HCT116 cells.

45 ffect on cell growth and c-Myc expression in HCT116 cells.

46 bitor p21 (CDKN1A) was regulated by LRH-1 in HCT116 cells.

47 tors of VEGFR2 and AKT induced senescence in HCT116 cells.

48 owth rate in RKO cells but reduced growth in HCT116 cells.

49 n factors such as RUNX1, RUNX2, and MEF2C in HCT116 cells.

50 and AKT, resulting in inactivation of p21 in HCT116 cells.

51 irmed with submicromolar IC50 values against HCT116 cells.

52 FCRC was confirmed in functional assays with HCT116 cells.

53 een pRB and p53 inactivation was observed in HCT116 cells.

54 hromosome condensation 1 and SET proteins in HCT116 cells.

55 Cu(GTSC) and Cu(GTSCHCl) induce apoptosis in HCT116 cells.

56 DNMT1-/- or DNMT3B-/- human colon carcinoma (HCT116) cells.

57 l human cancer cell lines including H460 and HCT116(+/+) cells.

58 hRpn13 deletion from HCT116 cells abrogates RA190-induced accumulation of sub

59 ion, overexpression of miR-143 or miR-145 in HCT116 cells abrogates signaling through the MAPK, PI3K

60 tingly, chromosome 3 transfer into MSH3-null HCT116 cells activated an alternative, MSH3-like activit

61 In HCT116 cells, ADI-PEG20 inhibited hypoxic-activation of

62 Notably, regions that are open in both HCT116 cells after treatment and in DKO1 cells include p

63 lon cancer HCT116 cells with JKA97 inhibited HCT116 cell anchorage-independent growth in vitro and tu

64 g of sodium bisulfite treated total DNA from HCT116 cells and analysis of genome-wide sodium bisulfit

65 C(50) values <1 muM for growth inhibition of HCT116 cells and approximately 1 muM for SW480 cells, as

66 Cytokine secretion from HCT116 cells and cellular migration were attenuated by i

67 Similar results were observed in transgenic HCT116 cells and embryonic fibroblasts from MMP-9-/- mic

68 e analyzed subcellular fractions of HeLa and HCT116 cells and found a significant increase in nuclear

69 -methyl-2'-deoxycytidine content in parental HCT116 cells and in HCT116 cells where DNMT3b was geneti

70 lation of CDKN2A promoter in colon carcinoma HCT116 cells and its reactivation after 7 days of treatm

71 1mt KO fibroblasts and human colon carcinoma HCT116 cells and measured mtDNA after 3-d treatment with

72 lass of COMPASS family members in both human HCT116 cells and mouse embryonic stem cells and find tha

73 interacted with the Bcl-w promoter in intact HCT116 cells and mutation of this site significantly dec

74 eted a CRC risk-associated H3K27Ac peak from HCT116 cells and observed large-scale changes in gene ex

75 e compounds inhibited growth and survival of HCT116 cells and produced the polyploid cellular phenoty

76 n was predominantly nuclear in proliferating HCT116 cells and relocalized to the cytoplasm after cell

77 Chromatin immunoprecipitation (ChIP) in HCT116 cells and their hypermethylated variant showed th

78 ax-deficient cell lines, including DU145 and HCT116 cells and those cell lines expressing low levels

79 This method works in both HCT116 cells and U2OS cells and can easily be scaled up

80 in wild type p53 compared with p53-deficient HCT116 cells, and also sensitizes tumour cells to doxoru

81 n 616 (N616fs*) in one of the VCP alleles in HCT116 cells, and we showed that this mutant allele is s

82 much less effect on p53-null H1299 cells and HCT116(-/-) cells, and importantly no toxicity on normal

83 HCT116 cells are heterozygous for beta-catenin (HCT116(W

84 HCT116 cells are heterozygous for gain of function mutan

85 yotype analyses revealed that DNMT-deficient HCT116 cells are highly unstable with respect to large-s

86 er activity and PKCbetaII mRNA expression in HCT116 cells are inhibited by the selective PKCbeta inhi

87 Both HCT116+chr2 and parental HCT116 cells (as well as HEC59 and ACVR2 and hMSH2 compl

88 p220 is required for proliferation of HCT116 cells, as assessed after expression of Cre recomb

89 t IP6K inhibitors were incubated with intact HCT116 cells at concentrations of 2.5 muM; diosmetin was

90 on factor 4 (Tcf4) signaling pathway using a HCT116 cell-based luciferase reporter assay.

91 Myc transcription is negligible in quiescent HCT116 cells but is induced when cells reenter the cell

92 tural p53 binding site, was methylated in WT HCT116 cells but not in DNMT1 null or p53 null cells.

93 5C and Cdc2 were down-regulated in wild-type HCT116 cells but not in p53-null, DNMT1-null or DNMT1and

94 ficantly enhanced PUMA-mediated apoptosis in HCT116 cells but not in PUMA-knockout cells.

95 death in K-ras-activated human colon cancer HCT116 cells but not in the K-ras-disrupted HCT116-deriv

96 dissociated preferentially from Bcl-X(L) in HCT116 cells but not in the PUMA-knockout cells, in resp

97 synergistic in p53-null but not in parental HCT116 cells by median effect/combination index analysis

98 und that apoptosis was induced in DNMT1(+/+) HCT116 cells by only a limited range of doxorubicin dose

99 ty induced in cultured human colon carcinoma HCT116 cells by the antitumor radiomimetic enediyne anti

100 onditioned medium from F. nucleatum-infected HCT116 cells caused naive cells to migrate, which was bl

101 In HCT116 cells, ceRNA depletion resulted in decreased PTEN

102 Although the mutation rate in HCT116 cell clones (6.2 x 10(-4)) was 30 times higher th

103 gulation of survival and metastatic genes in HCT116 cells compared to HCT116b cells.

104 27 interferon-inducible genes was reduced in HCT116 cells compared with the isogenic clones with targ

105 ckdown of Bak in Bax-deficient cells renders HCT116 cells completely resistant to apoptosis induction

106 transcriptome, and phenotypic differences of HCT116 cells containing a wild-type (HCT116-WT) or mutan

107 ng radiation is comparable with that seen in HCT116 cells containing Chk2, indicating that Chk2 is no

108 eduction in phosphocholine in MDA-MB-231 and HCT116 cells correlated positively with the drop in P-ER

109 H2AX increases after camptothecin removal in HCT116 cells deficient for p53 (p53-/-) or p21(CDKN1A) (

110 ease from the mitochondria to the cytosol in HCT116 cells, demonstrating that the compound induces ap

111 HCT116 cells depleted of IP6K2 are resistant to cell dea

112 kinase (IP6K) 1 and IP6K2 to generate human HCT116 cells devoid of any inositol pyrophosphates.

113 We report that Claspin-depleted HeLa and HCT116 cells display levels of replication fork slowing

114 strate that LRH-1-mediated p21 regulation in HCT116 cells does not involve altered p53 protein or pho

115 tation experiments performed on H2O2-treated HCT116 cells, endogenous MLK3 associated with endogenous

116 y function through analysis of human somatic HCT116 cells engineered to contain a conditional p220 al

117 bsequent studies using p53(+/+) and p53(-/-) HCT116 cells established that lucanthone induced catheps

118 hibited by small interfering RNA, irradiated HCT116 cells exhibited increased mitotic indices and a r

119 ptotic stimulation, most Bak in unstimulated HCT116 cells exists in two distinct protein complexes, o

120 Both wild-type and Bax-deficient HCT116 cells expressed the 150-kDa form of Bcl-xL, which

121 as demonstrated further in BAX/BAK-deficient HCT116 cells expressing a P168A mutant of BAX.

122 In HCT116 cells expressing a wild-type PPARgamma, troglitaz

123 Finally, we demonstrated that HCT116 cells expressing dominant negative TCF4 (dnTCF4)

124 5-Fluorouracil treatment of colon carcinoma HCT116 cells expressing WT p53 results in a reduction of

125 In contrast, in HCT116 cells, Fibulin 3 promotes migration and invasion

126 eted, which was attenuated in the Dicer(Ex5) HCT116 cells (Figure 5B; Tay et al., 2011).

127 pase 9 inhibition only rescued the wild-type HCT116 cells from death induced by TRAIL.

128 wth-limiting conditions, (a) GSTP1 protected HCT116 cells from oxidative stress and associated apopto

129 both CPT-11 pretreated wild-type and Bax-/- HCT116 cells from TRAIL-induced apoptosis, whereas caspa

130 xy-camptothecin converted TRAIL signaling in HCT116 cells from type II to type I.

131 the helicase domain of both Dicer alleles in HCT116 cells generating an in-frame 43-amino-acid insert

132 In HCT116 cells, genetic knockout of DNMT1 caused moderate

133 demethylated HCT116 colon cancer cells with HCT116 cells genetically rendered hypomorphic for DICER,

134 Colorectal HCT116 cells have basal water and NH3 permeability, indi

135 Employing NCCIT and HCT116 cells, having high endogenous Wnt signaling, we o

136 Compared to HCT116 cells, HCT116p53(-/-) cells were more susceptible

137 In Bax-deficient HCT116 cells, however, THG specifically generates two ad

138 out or knockdown of mutant KRAS in DLD-1 and HCT116 cells impaired the hypoxic induction of only HIF-

139 ur independently generated CB-5083 resistant HCT116 cells, implying that the L526S mutation occurs in

140 nblastine, induced apoptosis of Bax-positive HCT116 cells in a p53-dependent manner; p53 was required

141 t and studied circulating human colon cancer HCT116 cells in response to a variety of magnitude of sh

142 f p21 achieved in both p53(+/+) and p53(-/-) HCT116 cells in response to pharmaceutical inhibition of

143 n innate immune molecule that is secreted by HCT116 cells in response to T. cruzi infection, inhibits

144 extracts prepared from exponentially growing HCT116 cells in the presence of ATP.

145 Using HCT116 cells in which MLL4 has also been knocked out, we

146 Similar results were obtained with HCT116 cells, in which the MMR deficiency was corrected

147 of the same genes that were downregulated in HCT116 cells, including the MYC oncogene.

148 We show that knockout of p53 in HCT116 cells increases expression of cytosolic HMGB1 and

149 topic expression of mutant R175H in p53-null HCT116 cells increases GRO1 expression.

150 promoter-dependent luciferase expression in HCT116 cells indicates that reactive oxygen species acti

151 pression by small interfering RNA (siRNA) in HCT116 cells induced growth inhibition and apoptosis in

152 In addition to HCT116 cells, inhibition of CHOP or DR5 induction also a

153 Similarly, in HCT116 cells, inhibition with 30 micromol/L U0126 caused

154 We found that in adherent 2D culture of HCT116 cells intracellular T and O2 are close to ambient

155 y revealed that polyploidization of p53(-/-) HCT116 cells is frequently accompanied by mitotic arrest

156 Elevated [ATP] in PPIP5K(-/-) HCT116 cells is underpinned by increased mitochondrial o

157 depletion reduced cell motility of HeLa and HCT116 cells, its overexpression triggered the activatio

158 In HCT116 cells, knockdown of CD95 enhanced sorafenib + vor

159 In human colon cancer HCT116 cells, knockdown of DR5 by siRNA blocked THG-indu

160 Real-time visualization of HCT116 cells labeled with green fluorescent protein-hist

161 Thus, in HCT116 cells, lapatinib adaptation can be mediated by al

162 microM) induces apoptosis in 73% of p53-null HCT116 cells (LD(50) 17.5 microM) as opposed to 17.6% of

163 94 expression in THBS1 retrovirus-transduced HCT116 cells, leading to decreased TSP-1 levels.

164 various human tumor cell lines including an HCT116 cell line (IC(50) = 0.08 microM).

165 enhancers by comparing the epigenomes of the HCT116 cell line and its highly demethylated derivative,

166 rgeting technique, we attempted to create an HCT116 cell line in which endogenous Chk1 is mutated so

167 Cisplatin-resistant clones of the HCT116 cell line underwent a prolonged G2 arrest after c

168 Cell viability of colon cancer HCT116 cell line was determined for a total of 23 organo

169 Based on the antiproliferative effect, HCT116 cell line was most sensitive to bean Azufrado Hig

170 y SP1 are more likely to be expressed in the HCT116 cell line we used, and SP1-bound CpG islands show

171 oduced different phosphosite motifs from the HCT116 cell line.

172 ale phosphoproteomics of the colon carcinoma HCT116 cell line.

173 In addition, using the isogenic HCT116 cell lines (p53+/+ and -/-), we show that the red

174 ion of the growth of MCF-7, A549, DU145, and HCT116 cell lines by 24a was observed, with respective I

175 between yeast and human cells, as HEK293 and HCT116 cell lines exhibit recruitment of the protein cha

176 Tests of the cytotoxicity on the THP-1 and HCT116 cell lines showed very low toxic effects.

177 nse of the p53 wild-type and p53-/- isogenic HCT116 cell lines, and found that the increase in splici

178 ly related to differential inhibition of the HCT116 cell lines.

179 ransformed hTERT-RPE1 and colorectal cancer (HCT116) cell lines and expressed the phosphatase in HeLa

180 selected three KRAS mutant (LS180, LoVo and HCT116) cell lines and two KRAS wild-type cell lines (SW

181 nerated Tet-On-inducible human colon cancer (HCT116) cell lines that express either the P1-driven (HN

182 STAT3 increased HCT116 cell migration and invasion up to fivefold, where

183 associated with CRC progression and promoted HCT116 cell migration.

184 on triggers G2/M arrest in the p53-wild-type HCT116 cells more than in the p53-null cells, and upregu

185 In contrast, HCT116 cells null for p53 were able to enter mitosis fol

186 In contrast, HCT116 cells null for the p53 alleles (HCT116 p53-/-) ex

187 coma cell line (LS141) and the p53 wild-type HCT116 cells, Nutlin-3a induced downregulation of E2F1 a

188 egardless of Se content, the cytotoxicity in HCT116 cells of both SeB forms appeared to be H2O2-indep

189 ngly, NCX1/3 regulated membrane potential of HCT116 cells only when alpha1D was silenced, and blockin

190 ectopically expressed in p21(Cip1)-deficient HCT116 cells, p21(Cip1), its family member p27(Kip1), an

191 lines derived from the colorectal carcinoma HCT116 cells: p53(+/+) (p53-wt), p53(-/-) (p53-null), p2

192 and cyclin-dependent kinase inhibitor p21 in HCT116 cells, particularly after genotoxic damage from d

193 EMT reversal and increases robustness in the HCT116 cells, permitting them to both form tumours and t

194 ysis revealed that CDK12 and CDK13 losses in HCT116 cells preferentially affect expression of DNA dam

195 T116 cells treated with LCA, CM derived from HCT116 cells pretreated with metformin and then treated

196 PTTG1 transfection into HCT116 cells prevented Aurora-A T288 autophosphorylation

197 study reported increased DU145 and wild-type HCT116 cell proliferation when these ceRNAs were deplete

198 inhibition with aminooxyacetic acid reduced HCT116 cell proliferation, migration, and invasion; redu

199 mpact DU145, wild-type HCT116, or Dicer(Ex5) HCT116 cell proliferation.

200 s for reinitiation of DNA synthesis, whereas HCT116 cells required only nutrient replenishment.

201 In addition, expression of c-Myb in HCT116 cells rescued cyclin B1 expression after B-myb ex

202 Here we show that colonic epithelial model HCT116 cells respond to Trypanosoma cruzi infection by s

203 Mre11 complementation in MRN-deficient HCT116 cells restored Chk2 activation as well as Rad50 a

204 troducing p53 plasmid DNA into p53-deficient HCT116 cells restored PUMA expression and apoptotic resp

205 eatment, knockdown of either TOPK or ERK2 in HCT116 cells resulted in a decreased phosphorylation of

206 noma cells, and overexpression of PCDHGC3 in HCT116 cells resulted in the reduction of colony formati

207 Knockdown of PPM1G in 293E and colon cancer HCT116 cells results in an increase in the phosphorylati

208 rt that the expression of Aldh1l1 in A549 or HCT116 cells results in the elevation of C16-ceramide an

209 Tumor xenografts of UCP2-overexpressing HCT116 cells retain growth in nude mice receiving chemot

210 Inducible knockdown in HCT116 cells reveals that PAT4 regulates a form of mTORC

211 evaluated and optimized with EpCAM-positive HCT116 cells seeded into whole blood.

212 c, and endoplasmic reticulum stress stimuli, HCT116 cells show clear-cut apoptotic sensitivities in t

213 Western blot analyses of irradiated HCT116 cells showed increased levels of p53, KLF4, and p

214 Consistently, PIK3CA mutant isogenic HCT116 cells showed increased resistance to cetuximab co

215 TGF-alpha antisense transfection of HCT116 cells showed that EGFR activation was due to incr

216 Lysates derived from MLN4924-treated HCT116 cells showed that whereas the beta-subunit of NAE

217 ecipitation of doxorubicin treated wild-type HCT116 cells showed the presence of DNMT1, p53, H3K9me2,

218 o growth factor-dependent HCT116b cells, the HCT116 cells showed up-regulation of TGF-alpha expressio

219 Knockdown of DPEP1 in SW480 and HCT116 cells significantly increased cell apoptosis and

220 In HCT116 cells, sorafenib + vorinostat treatment caused DI

221 ition also restored Rad50 and Nbs1 levels in HCT116 cells suggesting that Mre11 stabilizes Rad50 and

222 Experiments with HCT116 cells that are p53 +/+ (p53 wild-type) and -/- (p

223 raft tumours derived from human colon cancer HCT116 cells that contain wild type p53 compared with p5

224 removal of APC produced the same defects in HCT116 cells that have constitutively active beta-cateni

225 solated from wild-type and MMP-9-/- mice and HCT116 cells that were stably transfected with MMP-9.

226 In CHK2(-/-) HCT116 cells, the kinetics of Cdc25A degradation in resp

227 nduces caspase 3 activation and apoptosis in HCT116 cells through a Bax-dependent pathway.

228 THG) induces apoptosis of human colon cancer HCT116 cells through a Bax-dependent signaling pathway c

229 romotes in vitro and in vivo tumor growth of HCT116 cells through a mechanism dependent on p38alpha,

230 inhibit the Uba5 conjugation pathway in the HCT116 cells through formation of the Ufm1-ADS adduct.

231 E1B-55K probably underlies sensitization of HCT116 cells to anticancer drugs.

232 ac) restores the sensitivity of Bax-knockout HCT116 cells to apoptosis in response to THG treatment.

233 Knockdown of SphK2 sensitized HCT116 cells to apoptosis induced by doxorubicin with co

234 proteasome, we found deletion of UCHL5 from HCT116 cells to cause increased levels of ubiquitinated

235 s was observed in both p53(+/+) and p53(-/-) HCT116 cells to comparable levels.

236 ost of these E1B-55K mutants could sensitize HCT116 cells to etoposide and doxorubicin.

237 Decreased Ron expression sensitized HCT116 cells to growth factor deprivation stress-induced

238 eltaProAE, could also sensitize p53 knockout HCT116 cells to MDA-induced Bax activation and apoptosis

239 ducing the levels of Claspin and Timeless in HCT116 cells to pretumoral levels impeded fork progressi

240 ally sensitized stable R2-knockdown p53(-/-) HCT116 cells to the cytotoxicity of cisplatin and gamma-

241 significant change in the susceptibility of HCT116 cells to TRAIL-induced apoptosis.

242 mutant allele sensitized heterozygous mutant HCT116 cells to treatment.

243 ffect the bulk CTD phosphorylation levels in HCT116 cells, transcriptome sequencing (RNA-seq) analysi

244 In contrast to RII transfectants, HCT116 cells transfected with chromosome 3 (designated H

245 The RNA of HCT116 cells treated with CPT for various times was anal

246 red with conditioned media (CM) derived from HCT116 cells treated with LCA, CM derived from HCT116 ce

247 se in POX catalytic activity was obtained in HCT116 cells treated with troglitazone with a concomitan

248 In human colorectal carcinoma (HCT116) cells treated with H2O2, extracellular signal-re

249 ificantly more cytotoxic than oxaliplatin to HCT116 cells, triggering higher levels of caspase-3 and

250 Furthermore, in HCT116 cells two non-essential amino acids, glutamine an

251 tions arise in MMR-proficient and -deficient HCT116 cells undergoing selection for methotrexate resis

252 are elevated on direct delivery of ATP into HCT116 cells using liposomes.

253 NA interference (RNAi) targeting of DNMT1 in HCT116 cells validated the results seen using genetic kn

254 vels; sorafenib + vorinostat exposure killed HCT116 cells via an intrinsic pathway/caspase 9-dependen

255 increased TGF-alpha expression in quiescent HCT116 cells was associated with constitutive epidermal

256 High uptake of the complex into HCT116 cells was detected by luminescent confocal micros

257 hat H3S10 phosphorylation in HeLa, A549, and HCT116 cells was high during prophase, prometaphase, and

258 Doxorubicin uptake into colon HCT116 cells was measured using the drug's intrinsic flu

259 e cytotoxicity induced by selenocompounds in HCT116 cells was not associated with cellular H2O2 level

260 level of EGFR activation in growth-arrested HCT116 cells was only slightly higher than that of expon

261 Drug-induced DNA damage in HCT116 cells was revealed by induction of the histone ga

262 The growth factor independence of HCT116 cells was shown to be dependent on autocrine tran

263 Next, in intact HEK293 and HCT116 cells, we monitored the stability of a cadre of N

264 -dependent G(1)/S phase cell cycle arrest in HCT116 cells, we now demonstrate that this arrest respon

265 NA effect in microRNA deficient (Dicer(Ex5)) HCT116 cells, we observed increased PTEN protein levels.

266 Bax-deficient HCT116 cells were completely resistant to TRAIL regardle

267 Haspin knockout and Haspin inhibitor-treated HCT116 cells were hypersensitive to VX-680.

268 hMLH1 and ACVR2 mutant HCT116 cells were previously stably transferred with chr

269 Moreover, PUMA knockout HCT116 cells were resistant to MDA-induced Bax conformat

270 HT1080 and HCT116 cells were treated with either AdHIF-1alpha-no-TA

271 in the regulation of the stability of KLF4, HCT116 cells were treated with proteasome inhibitors.

272 chromatin immunoprecipitation experiments in HCT116 cells were used to characterize a conserved p53 r

273 dine content in parental HCT116 cells and in HCT116 cells where DNMT3b was genetically deleted.

274 e LRH-1-regulation of p21 was not evident in HCT116 cells where p53 had been deleted.

275 RNA accelerates tumor xenograft formation by HCT116 cells, whereas SirT1 overexpression inhibits tumo

276 tically impaired in Bax knock-out (Bax(-/-)) HCT116 cells, whereas the knock-out of p53 or PUMA did n

277 tically inhibited TRAIL-induced apoptosis in HCT116 cells, which are highly susceptible to TRAIL in n

278 ted NF-kappaB and induced IL-8 expression in HCT116 cells, which express both Nod1 and Nod2, but not

279 s in butyrate-induced apoptosis, we utilized HCT116 cells, which harbor an oncogenic k-ras mutation a

280 azone also induced p53 protein expression in HCT116 cells, which may be the possible mechanism for PP

281 following siRNA-mediated LRH-1 knockdown in HCT116 cells, which require LRH-1 for growth and in HT29

282 pases 8 and 3 in HT29 and HCTp5.2 but not in HCT116 cells, which we postulate to be the basis for hig

283 A methylation changes, human colon carcinoma HCT116 cells, which were hypomorphic for DNA methyltrans

284 deduced for TrkC-miR2 after the treatment of HCT116 cells with 5-azacytidine, which resulted in diffe

285 We also report that treatment of HCT116 cells with a combination of the G-quadruplex inte

286 Pretreatment of growth-arrested HCT116 cells with AG1478, a selective inhibitor of EGFR

287 peripheral nerve sheath (MPNST) and p53-null HCT116 cells with cisplatin (Cis) and Nutlin-3a induced

288 In HCT116 cells with constitutive E1B-55K expression, the a

289 Treatment of HCT116 cells with Decitabine (a DNMT inhibitor) or trich

290 HCT116 cells with E1B-55K expression displayed a cell cy

291 10-fold higher compared to that in parental HCT116 cells with functional wild-type p53.

292 und that co-incubation of human colon cancer HCT116 cells with JKA97 inhibited HCT116 cell anchorage-

293 Transfection of HCT116 cells with KLF5 or p53 attenuated the binding of

294 Prolonged incubation of HCT116 cells with lapatinib caused cell killing followed

295 Treatment of T98G and HCT116 cells with nocodazole alone resulted in a robust

296 xpressing dominant negative TCF4 (dnTCF4) or HCT116 cells with silenced Snail failed to stimulate IL1

297 as well as IC(50) values of 1.5-2.5 muM for HCT116 cells with the luciferase reporter assay.

298 Treating HCT116 cells with THG results in caspase-8 activation; B

299 In human colon carcinoma HCT116 cells with wild-type (wt) p53, gammaH2AX reverses

300 a significant G2/M phase arrest in T24T and HCT116 cells without affecting p53 protein expression an