ライフサイエンスコーパス: HCT116 cell

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

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

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

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

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

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

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

8 ome instability of spontaneous polyploids in HCT116 cells.

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

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

11 repression and induced growth inhibition in HCT116 cells.

12 uciferase transcription when introduced into HCT116 cells.

13 y which the kinase inhibitor lapatinib kills HCT116 cells.

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

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

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

17 ncreased NOS2 mRNA and protein expression in HCT116 cells.

18 3+/- and p53-/- isogenic clones derived from HCT116 cells.

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

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

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

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

23 tions are induced by oxaliplatin in parental 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 ffect on cell growth and c-Myc expression in HCT116 cells.

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

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

40 ated slowly by collagen in adherent T47D and HCT116 cells.

41 ither untreated or DNA damage-stressed human HCT116 cells.

42 o CPT-11 as compared with vector transfected Hct116 cells.

43 poptosis of the p53(-/-) HCT116 and p21(-/-) HCT116 cells.

44 ke active Chk2 from neocarzinostatin-treated HCT116 cells.

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

46 grin-mediated adhesion, and micromotility of 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 Cu(GTSC) and Cu(GTSCHCl) induce apoptosis in HCT116 cells.

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

56 candidate oxidoreductases were expressed in HCT116 cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 1mt KO fibroblasts and human colon carcinoma HCT116 cells and measured mtDNA after 3-d treatment with

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

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

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

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

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

78 ell cloning of purged and sorted GPI-anchor- HCT116 cells and sequencing of the PIGA gene in each clo

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

80 and maintenance of IR-induced G(2) arrest in HCT116 cells and their isogenic p53 (-/-) derivative, in

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

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

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

84 ell cycle arrest compared with MMR-deficient HCT116 cells, and asynchronous ME-10 cells demonstrated

85 ed that only one copy of MGMT gene exists in HCT116 cells, and the status of promoter methylation of

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

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

88 HCT116 cells are heterozygous for gain of function mutan

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

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

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

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

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

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

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

96 5C and Cdc2 were down-regulated in wild-type HCT116 cells but not in p53-null, DNMT1-null or DNMT1and

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

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

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

100 d cell cycle arrest and senescence of the wt HCT116 cells, but apoptosis of the p53(-/-) HCT116 and p

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

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

103 Inhibition of endogenous Drg1 expression in Hct116 cells by stable expression of an antisense (AS) D

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

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

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

107 27 interferon-inducible genes was reduced in HCT116 cells compared with the isogenic clones with targ

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

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

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

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

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

113 HCT116 cells depleted of IP6K2 are resistant to cell dea

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

115 Many other cell lines, including HCT116 cells, do not readily upregulate p53 in response

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

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

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

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

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

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

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

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

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

125 5-Fluorouracil treatment of colon carcinoma HCT116 cells expressing WT p53 results in a reduction of

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

127 apoptotic pathway, by Z-VAD-FMK, in p21(-/-) HCT116 cells following treatment with 20 nm CPT did not

128 1 was required for senescence development of HCT116 cells following treatment with low concentrations

129 Clonogenic survival of HCT116 cells following UV irradiation showed no dependen

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

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

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

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

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

135 In HCT116 cells, genetic knockout of DNMT1 caused moderate

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

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

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

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

140 UCN-01 inhibits Chk2 immunoprecipitated from HCT116 cells (IC(50), approximately 10 nM).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 We found that in human colon carcinoma HCT116 cells, IR treatment enhanced Chk2 kinase activity

158 optosis by SN-38 followed by flavopiridol in Hct116 cells is Drg1.

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

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

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

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

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

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

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

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

167 94 expression in THBS1 retrovirus-transduced HCT116 cells, leading to decreased TSP-1 levels.

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

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

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

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

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

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

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

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

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

177 nd the isogenic p53(-/-) HCT116 and p21(-/-) HCT116 cell lines with a high concentration (250 nm) of

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

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

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

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

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

183 In HCT116 cells, loss of p53 (HCT/p53(-/-)) or p21 (HCT/p21

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 Interestingly, HCT116 cells revealed a significant G2-M arrest but Hela

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

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

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

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

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

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

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

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

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

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

219 In HCT116 cells, sorafenib + vorinostat treatment caused DI

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

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

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

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

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

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

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

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

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

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

230 at FR increases the sensibility of H1299 and HCT116 cells to 5-fluorouracil-, doxorubicin- and H(2)O(

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

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

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

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

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

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

240 mutant allele sensitized heterozygous mutant HCT116 cells to treatment.

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

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

243 nt expression of p21 blocked apoptosis of wt HCT116 cells treated with 20 nm, but not 250 nm CPT.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 when xenografted in mice, AS Drg1-expressing Hct116 cells were 3-fold more sensitive to CPT-11 as com

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

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

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

266 For this purpose, HCT116 cells were stably transfected with an expression

267 MR)-proficient HCT116+chr3 and MMR-deficient HCT116 cells were transfected with pCMV-(CA)13-EGFP, a p

268 No significant mutations were detected when HCT116 cells were transfected with the pCMV-(N)26-EGFP c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 After treatment of HCT116 cells with a radiomimetic compound neocarzinostat

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

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

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

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

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

290 wever, subsequent treatment of SN-38-treated Hct116 cells with flavopiridol induced apoptosis.

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