ライフサイエンスコーパス: colon cancer cell

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

2 signal and redox state in human cervical and colon cancer cells.

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

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

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

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

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

8 inhibit proliferation and viability in human colon cancer cells.

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

10 ly antiproliferative against human ovary and colon cancer cells.

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

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

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

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

15 dherin and suppressed mesenchymal markers in colon cancer cells.

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

17 )-520g is correlated with drug resistance of colon cancer cells.

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

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

20 smembrane subunit induces TAK1 expression in colon cancer cells.

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

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

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

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

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

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

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

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

29 sely correlated with metastatic potential of colon cancer cells.

30 ytotoxic and antioxidative activity on human colon cancer cells.

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

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

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

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

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

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

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

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

39 heckpoint affected sensitivity to MLN4924 in colon cancer cells.

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

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

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

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

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

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

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

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

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

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

50 satellite instable and microsatellite stable colon cancer cells.

51 ely after intrasplenic injection of 50K MC38 colon cancer cells.

52 e with CH223191 reduced the proliferation of colon cancer cells.

53 cally regulates NUR77 to induce apoptosis of colon cancer cells.

54 n human primary hepatocytes and LS174T human colon cancer cells.

55 c RARbeta and NUR77, leading to apoptosis of colon cancer cells.

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

57 % of active MYC alleles at any given time in colon cancer cells.

58 tially explaining the decreased migration of colon cancer cells.

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

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

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

62 on of talin1 inhibited 3D spheroid growth in colon cancer cells.

63 d consequently inhibits the proliferation of colon cancer cells.

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

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

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

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

68 that 4-hydroxyacetophenone (4-HAP) inhibits colon cancer cell adhesion, invasion, and migration in v

69 iated mutations, we report that human HCT116 colon cancer cells also survive when ORC5 protein expres

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

71 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

72 he lamellipodial leading edges of HT29 human colon cancer cells and are colocalized with aquaporin-1

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 ell proliferation in patient-derived primary colon cancer cells and established CRC cell lines.

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

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

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

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

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

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

82 nhibitor JQ1 synergized with sulforaphane in colon cancer cells and suppressed tumor development effe

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

84 SLC7A5, SLC1A5, and AFMID were elevated in colon cancer cells and tissues, and kynurenine was signi

85 way caused preferential death of established colon cancer cells and transformed colonic organoids.

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

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

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

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

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

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

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

93 The alpha(v)beta(3) integrin receptors in colon cancer cells are successfully targeted and imaged

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

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

96 d the induction of migration and invasion of colon cancer cells, as well as their tumorigenicity in v

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

98 antibiotic use can promote tumorigenesis by colon cancer cells at the anastomosis after colorectal s

99 Moreover, C3G promoted colon cancer cell attachment to fibronectin.

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

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

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

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

104 ax as well as cleaved caspase-3 and -PARP in colon cancer cells by downregulating RSK1 and MSK2 downs

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

106 f APA profiles characteristic for metastatic colon cancer cells, by regulating poly(A) site selection

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

108 ctangular geometries of bio-printed 3D human colon cancer cell constructs.

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

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

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

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

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

114 Deletion of TET2 in p53-null colon cancer cells enhanced DNA damage and restored chem

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

116 deletion inhibits the growth of murine MC38 colon cancer cells, especially under detachment conditio

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

118 We show here that p53-deficient colon cancer cells exposed to tumor-like metabolic stres

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

120 and p120-catenin isoform switching in SW480 colon cancer cells: fl-APC increased the expression of g

121 Furthermore, GNL1 protects colon cancer cells from chemo-drug-induced apoptosis.

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

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

124 was also observed in acquired 5-FU resistant colon cancer cells (HCT116 5-FU Res).

125 proved antiproliferative selectivity against colon cancer cells (HCT116 p53(+/+) ) with respect to th

126 domain supports UHRF1 oncogenic activity in colon cancer cells, highlighting that UHRF1 SRA antagoni

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

128 city and antiproliferative activity on human colon cancer cells (HT29).

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

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

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

132 nst various human cancer cells, killing SW48 colon cancer cells in particular with a submicromolar ha

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

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

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

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

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

138 4% enhancement in co-localization with SW-48 colon cancer cells in vitro, while influencing nanogel u

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

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

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

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

143 Preliminary data also show that HCT-116 colon cancer cells, in which hMATE1 is epigenetically re

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

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

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

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

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

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

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

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

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

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

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

155 acing glutamate with glutamine renders human colon cancer cells largely resistant to ceramide-induced

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

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

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

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

160 d exhibits antiproliferative efficacy in the colon cancer cell line COLO 320DM in vitro.

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

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

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

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

165 We performed Protect-seq on the human colon cancer cell line HCT-116 and observed overlap with

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

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

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

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

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

171 A colon cancer cell line with RNF43-G659Vfs*41 and BRAF-V6

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

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

174 3K and MAPK pathways in isogenic models of a colon cancer cell line, it generates plausible network h

175 A human colon cancer cell line, RNA silencing, and pharmacologic

176 spots are not evident in a poorly migrating colon cancer cell line, SW620, which lacks comparable me

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

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

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

180 yed strong anticancer activity against HT-29 colon cancer cell line.

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

182 way was affected in an oxaliplatin resistant colon cancer cell line.

183 y in the submicromolar range against a human colon cancer cell line.

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

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

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

187 tion of TASIN analogues and activity against colon cancer cell lines and an isogenic cell line pair r

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

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

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

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

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

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

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

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

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

197 In vivo, SHH interference in colon cancer cell lines decreased primary tumor growth a

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

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

200 ars to be representative of a broad panel of colon cancer cell lines harboring mutant KRAS.

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

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

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

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

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

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

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

208 as well as several Ras mutations in lung and colon cancer cell lines on fast 10 min gradient separati

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

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

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

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

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

214 or knockdown in 10 upper gastrointestinal or colon cancer cell lines with KRAS mutations or amplifica

215 man colon cancer specimens, human and murine colon cancer cell lines, and FXR transgenic mice, here w

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

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

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

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

220 14 against cancer cell growth in bladder and colon cancer cell lines, which provides valuable informa

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

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

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

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

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

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

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

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

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

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

231 ng exon alpha (105-nucleotide) in normal and colon cancer cell lines.

232 116, SW480, and HT-29) and one mouse (CT26) colon cancer cell lines.

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

234 1 in YAMC mouse colonocytes and Caco-2 human colon cancer cell lines.

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

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

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

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

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

240 he 5' MMP7 promoter, an event that inhibited colon cancer cell proliferation and invasion.

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

242 Since COX-2 and PGE(2) signaling can impact colon cancer cell proliferation and survival, we examine

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

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

245 While C3G had no significant effect on colon cancer cell proliferation, it significantly inhibi

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

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

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

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

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

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

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

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

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

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

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

257 xpression and knock-down studies of FOXM1 in colon cancer cells suggest the importance of FOXM1 in TY

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

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

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

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

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

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

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

273 e probe Sabrina Heng Lithium (SHL) in living colon cancer cells to noninvasively monitor cation chann

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

277 CCAR2) as an early target for acetylation in colon cancer cells treated with sulforaphane.

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

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

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

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

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

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

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

285 with normal human colonic epithelial cells, colon cancer cells were more sensitive to the depletion

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 ho and RalA/B signaling in mut-KRAS lung and colon cancer cells with little effect on wild-type (wt)-