ライフサイエンスコーパス: colon cancer cell

1 mbined and tested for cytotoxicity in CaCo-2 colon cancer cells.

2 )-520g is correlated with drug resistance of colon cancer cells.

3 n isogenic KRAS HCT116 and mutant KRAS SW620 colon cancer cells.

4 e ERK activity and growth in human liver and colon cancer cells.

5 smembrane subunit induces TAK1 expression in colon cancer cells.

6 NMTs in silencing these key silenced TSGs in colon cancer cells.

7 itive feedback loop enhances the invasion of colon cancer cells.

8 ntial apoptosis in LNCaP prostate and HCT116 colon cancer cells.

9 proliferation and adhesion in RKO and KM12SM colon cancer cells.

10 ays to further elucidate the effect of CA in colon cancer cells.

11 ted drug efflux in multidrug-resistant human colon cancer cells.

12 nscriptional activity in p53-deficient human colon cancer cells.

13 d cultures and tumor xenografts derived from colon cancer cells.

14 ersist for up to 6 h were detected in HCT116 colon cancer cells.

15 sely correlated with metastatic potential of colon cancer cells.

16 crease NOX1 expression stably in HT-29 human colon cancer cells.

17 ytotoxic and antioxidative activity on human colon cancer cells.

18 of FL118 to inhibit clonogenic potential of colon cancer cells.

19 of candidate therapies of this type in human colon cancer cells.

20 EY) with antiproliferative activity on human colon cancer cells.

21 d suppressed Wnt-mediated gene expression in colon cancer cells.

22 tion of HDAC1 and HDAC2 promoter activity in colon cancer cells.

23 ptosis-resistant than in apoptosis-sensitive colon cancer cells.

24 LPA transcriptionally induced HIF-1alpha in colon cancer cells.

25 minant role in the suppression of EMT of the colon cancer cells.

26 heckpoint affected sensitivity to MLN4924 in colon cancer cells.

27 were conducted using HCT 116 and HT-29 human colon cancer cells.

28 Ralpha led to reduced OPN expression in HT29 colon cancer cells.

29 d consequently inhibits the proliferation of colon cancer cells.

30 us decreasing fuel energy in both normal and colon cancer cells.

31 ptosis-resistant but not apoptosis-sensitive colon cancer cells.

32 an effector of LPA-induced proliferation of colon cancer cells.

33 ntly of acquired resistance to 5-FU in human colon cancer cells.

34 ion, we investigated the protein partners in colon cancer cells.

35 ed NF-kappaB activation via cIAP2 in HCT 116 colon cancer cells.

36 asing cell proliferation in human and murine colon cancer cells.

37 ized TNF to suppress caspase-8 activation in colon cancer cells.

38 X, G and E on cell growth were found in both colon cancer cells.

39 hat DDB2 is a master regulator of EMT of the colon cancer cells.

40 that LPA stimulates HIF-1alpha expression in colon cancer cells.

41 ompounds was examined on the growth of HT-29 colon cancer cells.

42 ndle poison in normal colonic epithelial and colon cancer cells.

43 directly inhibits the expression of Bmi1 in colon cancer cells.

44 hat triggers AIF/EndoG-mediated apoptosis in colon cancer cells.

45 hesion and reduces the invasive potential of colon cancer cells.

46 eased beta-catenin protein in HCT116 and RKO colon cancer cells.

47 dependent accumulation of the fluorophore in colon cancer cells.

48 fects of the combination chemotherapy on the colon cancer cells.

49 ct of WNT activity on stemness phenotypes in colon cancer cells.

50 cisplatin and oxaliplatin resistance in LoVo colon cancer cells.

51 expression and a stall in the growth of DLD1 colon cancer cells.

52 dhesion in normal adult crypt stem cells and colon cancer cells.

53 y contributing to the oncogenic phenotype of colon cancer cells.

54 owth arrest and a metabolic reprogramming in colon cancer cells.

55 mbined and tested for cytotoxicity in CaCo-2 colon cancer cells.

56 compared with TRAIL-sensitive human lung and colon cancer cells.

57 NA) contribute to the stem-like character of colon cancer cells.

58 tion factors, Slug and ZEB1, in HCT116 human colon cancer cells.

59 decreased WASF3 protein levels in breast and colon cancer cells.

60 ly antiproliferative against human ovary and colon cancer cells.

61 e invasive capacity of breast, prostate, and colon cancer cells.

62 tially explaining the decreased migration of colon cancer cells.

63 R5 induction and FADD-dependent apoptosis in colon cancer cells.

64 s-1-mediated transcriptional upregulation in colon cancer cells.

65 d that it is frequently upregulated in human colon cancer cells.

66 dherin and suppressed mesenchymal markers in colon cancer cells.

67 performed for (99m)Tc-TCP-1 in human HCT116 colon cancer cells.

68 s, mitotic arrest was more pronounced in the colon cancer cells (50% versus 10%).

69 ved the antiproliferative effects of 5-FU on colon cancer cells, accompanied by a reduction of in vit

70 In human colon cancer cells, activation of beta-catenin signaling

71 tructure to compare the landscapes of HCT116 colon cancer cells and a DNA methylation-deficient deriv

72 h an IC(50) of 24.43 microM in HCT-116 human colon cancer cells and an IC(50) of 25.82 microM in H-12

73 LGR5 ablation in colon cancer cells and crypt stem cells resulted in loss

74 of anthocyanin-rich plant extracts on human colon cancer cells and determine their mechanism of acti

75 We tested these for function in human colon cancer cells and Drosophila embryos.

76 that Sox21 was sufficient to repress Cdx2 in colon cancer cells and in pluripotent stem cells.

77 (PKG2) to activate forkhead box O (FoxO) in colon cancer cells and in the colon epithelium of mice.

78 is associated with increased invasiveness of colon cancer cells and increased expression of MMP7 and

79 PAF is specifically overexpressed in colon cancer cells and intestinal stem cells and is requ

80 tant for polarization and differentiation of colon cancer cells and is frequently inactivated in colo

81 gate the factors that alter HGF signaling in colon cancer cells and its effects on cell proliferation

82 HepG2 hepatocellular carcinoma cells, HCT116 colon cancer cells and LNCaP and DU145 prostate cancer c

83 oter in HT1080 fibrosarcoma cells and HCT116 colon cancer cells and NME2-mediated transcriptional rep

84 increased proliferation and motility of both colon cancer cells and normal fibroblasts, increased the

85 KIT signaling promotes growth of colon cancer cells and organoids in culture and xenograf

86 ucdhl inhibited low-density proliferation of colon cancer cells and reduced tumor formation in nude m

87 ment leads to increased activin secretion in colon cancer cells and TGF-beta induced cellular migrati

88 Colon cancer cells and tissue displayed COX-2 mRNA level

89 firmed by coimmunoprecipitation in the HT115 colon cancer cells and was supported by a partial coloca

90 a key role in their anti-tumor activities in colon cancer cells and xenografts through the DR5, FADD

91 nhibited growth and tumorigenic potential of colon cancer cells, and DBC1 expression correlated with

92 n of beta-catenin and proliferation of human colon cancer cells, and increased tumor growth in mice.

93 nd protein abundance twofold in HCT116 human colon cancer cells, and induction was further enhanced (

94 lation and down-regulate Wnt target genes in colon cancer cells, and most restore Wnt regulation in D

95 cleus of primary colorectal tumors and human colon cancer cells, and oncogenic activation of Ras was

96 cytotoxicity to Caco-2, HT-29, HCT-116 human colon cancer cells, and reduced inflammatory response ca

97 RK-RSK phosphorylation as well as increasing colon cancer cell apoptosis through regulation of the ab

98 We found that metastatic colon cancer cells are able to transfer their amoeboid p

99 sodium butyrate promotes differentiation of colon cancer cells as evidenced by induced expression an

100 lassification of white blood T-cells against colon cancer cells, as well as lipid accumulating algal

101 MYC-nick promotes the migration of colon cancer cells assayed in 3D cultures or grown as xe

102 Thus, NFATc1 regulates colon cancer cell behavior and its transcriptional targe

103 In human colon cancer cells, blockade of IDO1 activity reduced nu

104 EK2 transcript levels were reduced in HCT116 colon cancer cells but not in isogenic p53(-/-) cells.

105 hanced cancer cell killing in cultured human colon cancer cells, but also improved antitumor activity

106 transcriptional function of beta-catenin in colon cancer cells by recruiting EZH2 to the coactivator

107 ell lines from stomach (AGS, MKN-28) and one colon cancer cell (Caco-2), and compared with the effect

108 bination chemotherapies in three-dimensional colon cancer cell cultures, or spheroids.

109 Myc-nick also delays colon cancer cell death after treatment with chemotherap

110 Moreover, TNKS inhibition in colon cancer cells decreases beta-catenin signaling, whi

111 Moreover, MYC-nick is elevated in colon cancer cells deleted for FBWX7, which encodes the

112 s well as stemness and high clonogenicity in colon cancer cells, depend on Wnt signaling to beta-cate

113 Here we show that human colon cancer cells depleted of Rap1GAP are endowed with

114 operatively with TGFbeta type II receptor in colon cancer cells, enhancing TGFbeta-mediated growth in

115 f exosomes is affected by differentiation of colon cancer cells; exosomes might be used by differenti

116 Furthermore, colon cancer cells expressing a cleavage-resistant form

117 y searching for genes up-regulated in HCT116 colon cancer cells genetically disrupted for DNMT1 (DNMT

118 c expression of miR-502 inhibited autophagy, colon cancer cell growth and cell-cycle progression of c

119 hibited anchorage-dependent and -independent colon cancer cell growth by reducing ERK-RSK phosphoryla

120 Colon cancer cell growth inhibition was accompanied by d

121 demonstrate that YHL-14 inhibits bladder and colon cancer cell growth through up-regulation of p21 ex

122 ypes, we reconstituted its signaling axis in colon cancer cells harboring MLK4-inactivating mutations

123 d the metastatic dissemination capability of colon cancer cells HT29, including the migration and inv

124 JMJD2B enhanced subcutaneous tumor growth of colon cancer cells in a p53-dependent manner, and geneti

125 matous polyposis coli/beta-catenin wild-type colon cancer cells in a paracrine fashion, whereas no hy

126 DNMT inhibition in reducing the viability of colon cancer cells in correlation with reactivation of T

127 ole of p53 dynamics in fractional killing of colon cancer cells in response to chemotherapy.

128 g of DCLK1 triggered apoptotic cell death of colon cancer cells in vitro and in vivo, and abolished c

129 red clonogenic potential in low Wnt activity colon cancer cells in vitro and in vivo.

130 of IRE1alpha suppressed the proliferation of colon cancer cells in vitro and xenograft growth in vivo

131 han its major constituents- proliferation of colon cancer cells in vitro, attenuated migration and do

132 er cell growth and cell-cycle progression of colon cancer cells in vitro.

133 Flavonoids inhibit the growth of colon cancer cells in vitro.

134 rogenitor cell compartment of growth-fueling colon cancer cells in vivo Our results imply that differ

135 ockdown and suppresses the tumorigenicity of colon cancer cells in vivo.

136 e in cell proliferation and tumorigenesis of colon cancer cells in vivo.

137 CDC37 overexpression in human colon cancer cells increased CDK4 protein levels, which

138 re, we reveal that silencing GUCY2C in human colon cancer cells increases Akt-dependent TGF-beta secr

139 and pharmacological inhibition of nCDase in colon cancer cells increases ceramide, and this is accom

140 y differentiated and highly metastatic SW620 colon cancer cells induced epithelial characteristics an

141 We show that activation of PKG2 in colon cancer cells inhibited cell proliferation, inhibit

142 t, forced expression of MITF in melanoma and colon cancer cells inhibited EGFR and conferred sensitiv

143 r to results that our group has published in colon cancer cells, inhibition of ERK phosphorylation in

144 we show that overexpression of caveolin-1 in colon cancer cells inhibits oxidant-induced activation o

145 onstrated decreased oxidative-stress induced colon cancer cell invasion, but increased interaction wi

146 ium butyrate-induced differentiation of HT29 colon cancer cells is associated with a reduced CD133 ex

147 ction of the mechanism of action of SPRY2 in colon cancer cells is important to understand the upregu

148 Similarly, in HT-29 colon cancer cells, isorhamnetin inhibited oncogenic Src

149 nd Rho/Rho kinase signaling in A431 and DiFi colon cancer cells, leading to phosphorylation of filami

150 Stimulation of LD density in human colon cancer cells led to a PI3K-dependent loss of FOXO3

151 Here we show that silencing p53 in colon cancer cells led to increased expression of Aha1,

152 een the theory and experiments using a human colon cancer cell line (COLO205) as the capture targets.

153 sal cytosolic Ca(2+) concentration of HCT116 colon cancer cell line and modified the cytosolic Ca(2+)

154 isplayed significant synergy in a metastatic colon cancer cell line and was effective in a MTX-transp

155 In vitro experiments were performed with colon cancer cell line Colo320 (high Nrp-2 expression) a

156 pression of LMNB1 by RNA interference in the colon cancer cell line DLD-1 and showed a dramatic redis

157 pen reading frames in a human KRAS-dependent colon cancer cell line engineered to express an inducibl

158 was tested by confocal microscopy in a human colon cancer cell line exclusively expressing Nox1 (HT-2

159 ze the genome-wide hnRNPK-DNA interaction in colon cancer cell line HCT116.

160 ncluding breast cancer cell line MDA-MB-231, colon cancer cell line HT-29, hepatocellular carcinoma c

161 ished by intrasplenic injection of the human colon cancer cell line LS174t.

162 t of liver cancer cell lines HepG2 and Huh7, colon cancer cell line RKO, and breast cancer cell line

163 tutive expression of RV-cyclin in the HCT116 colon cancer cell line significantly increases the level

164 mediated genome editing in a patient-derived colon cancer cell line suppressed anchorage-independent

165 consisting of four defined derivatives of a colon cancer cell line that resulted from consecutive ep

166 sed significantly by UbV.7.2 expression in a colon cancer cell line that was treated with the chemoth

167 potential PTK6 substrates in the human SW620 colon cancer cell line using mass spectrometry, includin

168 ability to inhibit the proliferation of the colon cancer cell line, HCT-116, in vitro, DNA damage an

169 ct with the DNA methyltransferase DNMT1 in a colon cancer cell line, HCT116.

170 ersistent MAPK activation in the SW620 human colon cancer cell line.

171 nsport and biosynthesis of terpenoids in the colon cancer cell line.

172 , we used CRISPR to KO PPIP5Ks in the HCT116 colon cancer cell line.

173 ty and induced apoptosis in the HCT116 human colon cancer cell line.

174 els could be modeled in an APC-mutated human colon cancer cell line.

175 te rapid cell migration in a AQP1-expressing colon cancer cell line.

176 fied as curcumin binding targets from HCT116 colon cancer cell line.

177 FAM120A was overexpressed in human colon cancer cell lines and 55% of human colon cancer sp

178 carcinoma proliferation, a) in vitro against colon cancer cell lines and b) in vivo on tumor growth i

179 uantify AKT1 and AKT2 from breast cancer and colon cancer cell lines and flash-frozen tumor lysates w

180 Knockdown of KIT decreased proliferation of colon cancer cell lines and growth of xenograft tumors i

181 ssion was associated with Jagged1 in various colon cancer cell lines and in tissues from colon cancer

182 o bisabolane derivatives were active against colon cancer cell lines and may be interesting as lead s

183 rase p300, whose levels are also elevated in colon cancer cell lines and patient samples.

184 adult glioma, IDH1 G97, which is mutated in colon cancer cell lines and pediatric glioblastoma, and

185 was observed in a significant proportion of colon cancer cell lines and primary colorectal tumors.

186 lasm and nuclei of several established human colon cancer cell lines and this localization pattern is

187 pression downstream of silenced NOX1 in both colon cancer cell lines and xenografts.

188 mutations, yet only a subset of KRAS mutant colon cancer cell lines are dependent upon KRAS signalin

189 ce as active towards pancreatic, breast, and colon cancer cell lines as its (R,R) enantiomer at 24 h.

190 rlotinib cotreatment on growth inhibition of colon cancer cell lines both as a result of enhanced inh

191 an up-regulate NKG2DL expression in multiple colon cancer cell lines by activating the ATM-Chk2-media

192 ntitation platforms to analyze a panel of 10 colon cancer cell lines differing by mutations in DNA mi

193 these compounds were evaluated against HT-29 colon cancer cell lines ex vivo.

194 his finding was confirmed in two independent colon cancer cell lines HCT116 (KRAS mutant) and HKe3 (K

195 Colon cancer cell lines HT29 (human) and MC26 (murine) w

196 Screening of a panel of 33 colon cancer cell lines identified cell lines sensitive

197 ease in protein phosphatase activity for two colon cancer cell lines in which NOX1 expression was kno

198 Evidence from knockout mice as well as colon cancer cell lines indicated that CDK2 is dispensab

199 APEX1 overexpression or knockdown in human colon cancer cell lines induced profound changes in mali

200 nt with this, LCT13 expression in breast and colon cancer cell lines is associated with silencing and

201 iated through KLF5 and identifies subsets of colon cancer cell lines responsive and refractory to thi

202 Induction of DACOR1 in colon cancer cell lines significantly reduced their abil

203 l cancer progression, we used three isogenic colon cancer cell lines that differ only in KRAS mutatio

204 we analyzed biological triplicates of eight colon cancer cell lines using the MultiNotch MS3 method.

205 d precise gene targeting to produce isogenic colon cancer cell lines with a knockout/rescue system fo

206 erlotinib synergistically inhibits growth of colon cancer cell lines, achieves promising efficacy in

207 ectors in DLD1, HT29, LS174T, and COLO320 DM colon cancer cell lines, and in UM-COLON#8 and POP77 xen

208 ione synthesis impaired survival of multiple colon cancer cell lines, and pharmacological targeting o

209 ified and validated in a panel of additional colon cancer cell lines, as well as the kinetics of syne

210 In colon cancer cell lines, Cdx2 directly regulated the tra

211 al drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116

212 antiproliferative activity against different colon cancer cell lines, opening the route to a new clas

213 Among colon cancer cell lines, those with KRAS mutations were

214 14 against cancer cell growth in bladder and colon cancer cell lines, which provides valuable informa

215 ted in migration assays using HT29 and SW480 colon cancer cell lines, with high and low levels of AQP

216 p21(KRAS) steady-state levels in mutant KRAS colon cancer cell lines.

217 oproliferative role for LRH-1 in established colon cancer cell lines.

218 affected Notch1 signaling in the breast and colon cancer cell lines.

219 eloma cell lines and was also active against colon cancer cell lines.

220 colonic epithelial cells, tumor tissues, and colon cancer cell lines.

221 a panel of colon tumors and patient-derived colon cancer cell lines.

222 ia, Dbait induced cytotoxicity in all tested colon cancer cell lines.

223 ice with colitis-associated cancer and human colon cancer cell lines.

224 d the effect of LPA on HIF-1alpha in several colon cancer cell lines.

225 combination, against the SW480 and RKO human colon cancer cell lines.

226 eir antiproliferative activity against HT-29 colon cancer cell lines.

227 1 in YAMC mouse colonocytes and Caco-2 human colon cancer cell lines.

228 of human colonic adenocarcinomas tested and colon cancer cell lines.

229 Loss of Cdx2 expression in colon cancer cells might reduce expression of Mucdhl and

230 Furthermore, GM-CSF stimulation renders colon cancer cells more resistant to cytotoxic agents.

231 nstrate that MMP-2 amplifies the motility of colon cancer cells, not only by digesting the extracellu

232 are a core determinant of chemoresistance in colon cancer cells, our findings may offer a foundation

233 g selective killing ability towards skin and colon cancer cells over their normal cell counterparts.

234 e sets related to glycolysis, hypoxia, and a colon cancer cell phenotype, including genes regulated b

235 ded the growth of xenografts from breast and colon cancer cells potentiated regression of the tumors

236 orticoid-regulated kinase 3 (SGK3), inhibits colon cancer cell proliferation and retards colon cancer

237 d RIP140 expression strongly repressed human colon cancer cell proliferation in vitro and after graft

238 down-regulated in colon cancer and inhibits colon cancer cell proliferation through CacyBP up-regula

239 te growth factor (HGF), reciprocally driving colon cancer cell proliferation through cMET-dependent s

240 nd intestinal stem cells and is required for colon cancer cell proliferation.

241 ed beta-catenin transcriptional activity and colon cancer cell proliferation.

242 pression or inhibition of GRM3 activation in colon cancer cells reduces cell survival and anchorage-i

243 erve that interference with Wnt signaling in colon cancer cells reduces glycolytic metabolism and res

244 beta-catenin, inhibited the proliferation of colon cancer cells, repressed colon CSCs and prevented x

245 Knockdown of THAP11 in SW620 colon cancer cells resulted in a significant decrease in

246 that inhibition of NFATc1 in human and mouse colon cancer cells resulted in decreased invasiveness in

247 Overexpression of CerS6 in HT29 colon cancer cells resulted in increased apoptotic susce

248 raft model, knockdown of endogenous PLAC8 in colon cancer cells resulted in smaller tumors, reduced l

249 We performed measurements on LoVo human colon cancer cells sensitive (LoVo-S) and resistant (LoV

250 Co-immunoprecipitation studies of colon cancer cells showed that the beta1 integrin subuni

251 Here we show that low adherent breast and colon cancer cells subpopulations have stem-like propert

252 trate that trypsin-sensitive (TS) breast and colon cancer cells subpopulations show increased ALDH ac

253 Reexpression of 15-LOX-1 in human colon cancer cells suppressed IL-6 mRNA expression, STAT

254 ce of TP53 genotype and let-7a inhibition on colon cancer cell survival following chemoradiation ther

255 this flavonoid shows anti-tumoral effects on colon cancer cells (SW480, DLD-1, and HCT116), whereas e

256 o suppress caspase-8 activation, but only in colon cancer cells that are resistant to tumor necrosis

257 n of the vitamin D receptor (VDR) pathway in colon cancer cells that expressed one of five CYP27B1 si

258 nt histone deacetylase inhibitors (HDACi) on colon cancer cells that harbor a GFP locus stably integr

259 t of acquired cross-drug resistance of human colon cancer cells that harbor different genetic backgro

260 ormation to identify H3K27Ac peaks in HCT116 colon cancer cells that harbor SNPs associated with an i

261 In renal epithelial cells and colon cancer cells, the choice of VEGF splice isoforms i

262 differentially regulates KLF4 in AML versus colon cancer cells through a mechanism that involves tis

263 naling leads to growth inhibition effects on colon cancer cells through the upregulation of several c

264 quantification of the invasion of spheroidal colon cancer cells through three-dimensional (3D) Matrig

265 KC also up-regulates cyclin D1 expression in colon cancer cells, through mechanisms that parallel tho

266 y, we test the hypothesis that PT sensitizes colon cancer cells to 5-FU and we examine the underlying

267 ds that potently increase the sensitivity of colon cancer cells to apoptotic ligands.

268 zing Dvl2 and potentiating Wnt signalling in colon cancer cells to ensure robust colon cancer progres

269 Knockdown of Sam68 sensitizes human colon cancer cells to genotoxic stress-induced apoptosis

270 Herein, we show that chronic exposure of colon cancer cells to GM-CSF, which harbor its receptor,

271 Ectopic expression of miR-192 sensitizes colon cancer cells to growth factor deprivation stress-i

272 Exposure of colon cancer cells to LL-37 induced phosphatidylserine e

273 downregulates BCL-XL and in turn sensitizes colon cancer cells to MEK inhibition.

274 bicin (DOX) sensitizes TRAIL-resistant HT-29 colon cancer cells to TRAIL by upregulating mRNA express

275 ribution of E-cadherin to plasma membrane in colon cancer cells transfected with miR-194.

276 of MMP-2 expression, as exemplified by HT29 colon cancer cells transfected with pCMV6-XL5-MMP-2.

277 Colon cancer cells treated with low-dose PEITC for >1 mo

278 .82%, and stable knockdown of SNRK increased colon cancer cell tumorigenicity.

279 by increased percentage of HCT-116 and HT-29 colon cancer cells undergoing apoptosis from 5.4% (untre

280 Here, we report that GRP78 is secreted from colon cancer cells via exosomes.

281 on growth and antioxidative status in human colon cancer cells was investigated in this study.

282 of primary tumors formed by murine and human colon cancer cells was reduced in mice by genetic or pha

283 lpha was necessary for LPA-induced growth of colon cancer cells, we determined the relationship betwe

284 y overexpressing the Wnt receptor, FZD-7, in colon cancer cells, we found that FZD-7 receptors expres

285 E), as well as of some phenolic standards on colon cancer cells were examined.

286 tive Oxygen Species (ROS) generation in both colon cancer cells, whereas apoptosis and ROS were not s

287 cantly increased the metastatic potential of colon cancer cells, whereas inhibition of NFATc1 reduced

288 nation and upregulation of PHLPP proteins in colon cancer cells, whereas knockdown of USP46 has the o

289 tion of LD density promoted proliferation in colon cancer cells, whereas silencing PLIN2 or overexpre

290 nt activated ERK1/2 and promoted invasion of colon cancer cells, which was attenuated by MLK3 siRNA k

291 n a luciferase knockdown study in HT29 human colon cancer cells, which were found to be more difficul

292 Treatment of colon cancer cells with 3-AP or 3-AP-Me activated all th

293 on 5-azadeoxy-cytidine (5-Aza) treated HT-29 colon cancer cells with an additional simulation study.

294 AK301 induced mitotic arrest in HT29 human colon cancer cells with an ED50 of approximately 115 nm.

295 ause cytotoxicity to HCT-116 and HT-29 human colon cancer cells with ED50 values of 134.4 and 217.0 m

296 Colon cancer cells with elevated PLAC8 levels exhibited

297 als in cells with exogenous reporters and in colon cancer cells with endogenously high Wnt activity.

298 and cleavage and growth suppression in human colon cancer cells with G12D or G12V mutations, thus ind

299 ze a reporter for Wnt activity and show that colon cancer cells with high levels of Wnt activity also

300 nergistically reduced the viability of human colon cancer cells with wild-type but not mutant KRAS ge