ライフサイエンスコーパス: HT29 cell

1 e role of exosomes in the differentiation of HT29 cells.

2 s, also inhibited MUC2 expression in induced HT29 cells.

3 /Sp3 binding, blocks MUC2 gene expression in HT29 cells.

4 l lines; however, TLR2 protein was absent in HT29 cells.

5 cells, p38 in T84 cells and MAPK and JNK in HT29 cells.

6 TR6 inhibited LIGHT-induced cytotoxicity in HT29 cells.

7 he effect of IGF-I induction of VEGF mRNA in HT29 cells.

8 engage the LTbetaR and trigger the death of HT29 cells.

9 ylate synthase but which sensitized only the HT29 cells.

10 th rhPG(1-80) increased the proliferation of HT29 cells.

11 lpha and MCP1 secretion in IEC18 and IL-8 in HT29 cells.

12 dhesive for E. coli O157:H7 binding to human HT29 cells.

13 lonogenic assay, 19 showed an HCR of 4090 in HT29 cells.

14 levated p21(Cip1), cyclin E, and cyclin A in HT29 cells.

15 ially rescued GANT61-induced cytotoxicity in HT29 cells.

16 he secretion of IL-8 in IFN-gamma pretreated HT29 cells.

17 e sodium butyrate-induced differentiation of HT29 cells.

18 L in RKO and HT29 cells and that of L-OHP in HT29 cells.

19 udin-1 protein expression in either SW480 or HT29 cells.

20 its robust induction by phase II inducers in HT29 cells.

21 were inhibited in SW480 but not in DLD-1 and HT29 cells.

22 e complex, interacts with endogenous NOD2 in HT29 cells.

23 experimentally established this in HepG2 and HT29 cells.

24 n IC(50) of approximately 0.25 micromol/L in HT29 cells.

25 role for HFE in inhibition of iron efflux in HT29 cells.

26 ckpoint mediators in FdUrd-treated SW620 and HT29 cells.

27 eated that express an activated MEK1 gene in HT29 cells.

28 ne catabolism and lower polyamine content in HT29 cells.

29 human hepatoma (HepG2) and colon carcinoma (HT29) cells.

30 ment, k(PL) remained below control levels in HT29 cells (74%, p = 0.02), and increased above treated

31 e expression of Fas and Fas ligand (FasL) on HT29 cells, a human colon adenocarcinoma cell line, and

32 microM) was minimally cytotoxic (20-30%) to HT29 cells after a 24-h exposure, and no dose response w

33 HCT116, SW480, and HT29 cells also expressed CSE1L protein.

34 HT29 cells also were incubated with the LXR ligand GW396

35 , or chk2 activation, which only occurred in HT29 cells and correlated with uracil misincorporation/m

36 cally altered human colon cancer cell lines, HT29 cells and Csk shRNA-transfected HT29 cells that exh

37 Nude mice were implanted with HT29 cells and fed with vehicle (carboxymethyl cellulose

38 nsfected Sik phosphorylates Sam68 in SNBs in HT29 cells and in the nucleoplasm of NMuMG cells.

39 agonist AG1024 were investigated in cultured HT29 cells and on the colonic epithelium of hGAS mice co

40 ng biotransformation of the two compounds in HT29 cells and propofol as an effective competitive inhi

41 ncorporation may reach a saturation point in HT29 cells and that a further increase in dUTP levels ha

42 d the cytotoxic activity of TRAIL in RKO and HT29 cells and that of L-OHP in HT29 cells.

43 2 phases in p53 mutant human colon carcinoma HT29 cells and that UCN-01 abrogates the S-phase arrest

44 umetanide-sensitive K+ (86Rb) uptake in both HT29 cells and the Cl--secreting T84 line.

45 um of intestinal epithelial cells (IEC18 and HT29 cells) and monocytes (THP-1 cells) and assessed the

46 12-O-tetradecanoylphorbol 13-acetate-induced HT29 cells, and Cl.16E cells, a clonal derivative of HT2

47 for similar periods of time, indicating that HT29 cells are not highly sensitive to induction of prog

48 STb binding to T84 and HT29 cells as a function of 125I-STb concentration did n

49 human colorectal cancer HCT116 (MLH1(+)) and HT29 cells as measured by LC3 immunoblotting, GFP-LC3 re

50 pectic samples reduced Stx2 cytotoxicity in HT29 cells, as measured by the reduction of human rRNA d

51 cleavage complexes in human colon carcinoma HT29 cells at the nucleotide level.

52 Generation of HK8 occurs in mitotic HT29 cells, basal crypt mitotic cells in normal mouse in

53 cytolytic activity was observed not only in HT29 cells but also in many other human cancer cell line

54 aside II (IC50 14 muM) impaired migration of HT29 cells but had minimal effect on SW480 cell migratio

55 ressed UGT protein at levels greater than in HT29 cells but with marked interpatient variations and p

56 anced the secretion of IL-8 and GRO-alpha in HT29 cells, but not in freshly isolated IEC cultures.

57 The capturing and regulating HT29 cells by the aSlex-coated dendrimer conjugate were

58 o specifically bind and capture colon cancer HT29 cells by using multiple Sialyl Lewis X antibodies (

59 cromolar concentrations of SKI-606 inhibited HT29 cell colony formation in soft agar.

60 In addition, purified intact nuclei from HT29 cells contained immunoreactive NQO1, which was cata

61 A subclone of HT29 cells containing numerous mucous granules and terme

62 ntained within a homogenate prepared from an HT29 cell culture.

63 LTbetaR, thereby suppressing LIGHT- mediated HT29 cell death.

64 The overexpression of nuclear PKM2 in HT29 cells decreased the effect of gefitinib therapy, wh

65 In contrast, depletion of dUTPase in HT29 cells did not substantially affect chemosensitivity

66 cation by 388 corresponded with reduction in HT29 cell DNA synthesis.

67 detect Acr-dG in calf thymus and human colon HT29 cell DNA with an excellent linear quantitative rela

68 ose of camptothecin in human colon carcinoma HT29 cells, DNA replication was inhibited rapidly and di

69 ex-FITC conjugate could specifically capture HT29 cells even when the target HT29 cells were diluted

70 Further, silencing of CK2alpha in HT29 cells following transfection of CK2alpha shRNA abro

71 d the Fas-ligand inhibitor failed to protect HT29 cells from CPT-induced apoptosis.

72 ant DN-Fas-associated death domain protected HT29 cells from TRAIL-induced apoptosis in the presence

73 that 125I-STb bound specifically to T84 and HT29 cells; however, the toxin-epithelial cell interacti

74 on of VEGF promoter-reporter constructs into HT29 cells, IGF-I increased the activity of the VEGF pro

75 the conjugate showed the enhanced capture of HT29 cells in a concentration-dependent manner and the m

76 so induces Top1cc in colon cancer HCT116 and HT29 cells in a time- and concentration-dependent fashio

77 ation sensitizer in studies carried out with HT29 cells in in vitro as well as in in vivo single and

78 by the inhibition of AP-1 binding in hypoxic HT29 cells in the presence of GA.

79 uced degradation of cdc25A in SW620, but not HT29 cells, in a manner that correlated with the previou

80 cells, which require LRH-1 for growth and in HT29 cells, in which LRH-1 does not regulate growth.

81 Butyrate treatment of intestinal epithelial HT29 cells induced a differentiation pattern that recapi

82 SU-a) rotavirus, and (iii) human intestinal (HT29) cells infected with SA11 were examined to determin

83 ulation by small interference RNA (siRNA) in HT29 cells inhibited Chk2 activation and down-regulated

84 vitro and in vivo when yCD was expressed in HT29 cells instead of bCD.

85 The invasion and adhesion of spheroidal HT29 cells is initiated by placing individual spheroids

86 Galectin-3, which is highly expressed in HT29 cells, is unique among galectins because it contain

87 he prodrugs were not effective adjuvants for HT29 cell killing.

88 y the HVEM-restricted virus, suggesting that HT29 cells lack a cofactor for HVEM-mediated infection o

89 the expression of dominant-negative Stat1 in HT29 cells led to the loss of growth inhibition in respo

90 ted from the SDS-PAGE gel generated from the HT29 cell line.

91 ly >50 microM) against colon HCT116 and lung HT29 cell lines but, unlike methylbenzoprim, this activi

92 CF7) and prostate cancer (PC3 mm2, A549, and HT29) cell lines.

93 start site was virtually methylation free in HT29 cells (Mer+), whereas in BE or HeLa S3 cells (Mer-)

94 We hypothesized that the antagonism in HT29 cells might be a consequence of altered p53 functio

95 In HT29 cells, mitomycin C treatment results in the inducti

96 anoikis; whereas decreased Src expression in HT29 cells (of high Src expression and activity) by tran

97 ionally expressing wild-type p53 activity in HT29 cells on DNA damage and cytotoxicity caused by expo

98 ) the capacity of necrotic cell lysates from HT29 cells or human IECs to induce human intestinal fibr

99 cant even at a low level of amplification in HT29 cells (P < 0.0001).

100 kinetics of cell death in IFN-gamma-treated HT29 cells paralleled the increase in the levels of Fas

101 IFN-gamma increase cellular plgAR levels in HT29 cells predominantly by activating protein tyrosine

102 at were purified from colonic cultured human HT29 cells pretreated with okadaic acid.

103 We found that, whereas HT29 cells progressed into S phase and demonstrated incr

104 Their effect on HT29 cell proliferation and cell migration was tested, a

105 In addition, expression of pdcd4 shRNA in HT29 cells promotes invasion.

106 Human platelets cocultured with HT29 cells rapidly adhered to cancer cells and induced C

107 HVEM cDNA isolated from HT29 cells rendered HSV-resistant cells permissive for i

108 ent of de-differentiated crypt-like DLD1 and HT29 cells resulted in enhanced expression of ICAM-1.

109 Oltipraz treatment of both HCT116 and HT29 cells results in the induction of proteins involved

110 utant in either HEK293 cells or colon cancer HT29 cells showed dramatically reduced NF-kappaB-activat

111 mechanisms of GANT61-induced cytotoxicity in HT29 cells showed increased Fas expression and decreased

112 ssociated cdc25A degradation are impaired in HT29 cells, signaling by ATM/ATR is intact upstream of c

113 Pet-intoxicated HEp-2 and HT29 cells stained with fluorescein-labeled phalloidin r

114 In HT29 cells studied further, rapid cleavage of caspase-8,

115 occupancy of the OPN promoter by ERRalpha in HT29 cells, suggesting that OPN is a direct target of ER

116 In contrast, knockdown of mutant BRAF in HT29 cells suppressed both HIF-1alpha and HIF-2alpha.

117 efficiently killed HCT116, DLD1, SW480, and HT29 cells than BBR3464, cisplatin, or oxaliplatin.

118 -201 and ONYX-203 replicated more rapidly in HT29 cells than wild-type Ad5, and they lysed HT29 cells

119 lines, HT29 cells and Csk shRNA-transfected HT29 cells that exhibit different degrees of neoplastic

120 s apoptosis of various tumor cells including HT29 cells that express both lymphotoxin beta receptor (

121 in vitro, MTA induced cell cycle effects on HT29 cells that resulted in potentiation of the cytotoxi

122 ls, and Cl.16E cells, a clonal derivative of HT29 cells that spontaneously differentiates into goblet

123 In contrast to these results, derivatives of HT29 cells that stably overexpressed p21Cip1/Waf1 displa

124 ominent levels of HK8 were also generated in HT29 cells that were induced to undergo apoptosis using

125 clin-dependent kinase inhibitor p27(kip1) in HT29 cells; this induction was attenuated by inhibition

126 itotic entry, suggesting that progression of HT29 cells through S phase during drug treatment results

127 ded the regrowth of fluoropyrimidine-treated HT29 cells to a greater extent in a well-differentiated

128 e inhibitor, increases the susceptibility of HT29 cells to anoikis in a dose- and time-dependent mann

129 we found that 5-Aza-CdR treatment sensitized HT29 cells to growth inhibition by exogenous IFN-alpha2a

130 icantly more sensitive to 5-FC in vitro than HT29 cells transduced with bCD (HT29/bCD).

131 HT29 cells, transfected with a plasmid containing green

132 ased coincident with S-phase accumulation in HT29 cells treated with ZD9331 or 5fluorouracil/leucovor

133 T29 cells than wild-type Ad5, and they lysed HT29 cells up to 1,000-fold more efficiently.

134 knocked down Pdcd4 expression in colon tumor HT29 cells using pdcd4 short hairpin RNA (shRNA).

135 pendent prostaglandin E2 (PGE2) synthesis in HT29 cells was involved in the downregulation of p21(WAF

136 e of the mutant strain to polystyrene and to HT29 cells was reduced by approximately 21% and 75%, res

137 Migration of human colon cancer (HT29) cells was assessed with a wound-closure assay in t

138 E using a monolayer of intestinal epithelial HT29 cells, we proved that HS loss directly causes prote

139 ally capture HT29 cells even when the target HT29 cells were diluted with the interfering cells (e.g.

140 T84 and HT29 cells were divided in several protocols: mesalamine

141 s of lexatumumab in TRAIL-resistant HCT8 and HT29 cells were dramatically augmented by the histone de

142 p21 regulation was not observed in HT29 cells, where p53 is mutated.

143 if any receptor), is moderately effective in HT29 cells (which express low levels of the receptor), b

144 e, we introduced a full-length DCC cDNA into HT29 cells, which can be induced in vitro to express MUC

145 int is defective in the relatively sensitive HT29 cells, which continue to progress through S phase d

146 inal kinase pathways and c-Jun expression in HT29 cells while exerting incomplete inhibitory effects

147 Differentiation of Caco2 and HT29 cells with 1alpha,25-dihydroxyvitamin D(3) or IFN-g

148 consequences of such binding, we transfected HT29 cells with a plasmid containing 3 kb of the DT-diap

149 Treatment of the 125I-STb-bound T84 and HT29 cells with an acidic saline solution to remove surf

150 ty of the VEGF promoter, and pretreatment of HT29 cells with dactinomycin abrogated the induction of

151 Treatment of HT29 cells with FasL or with the CH-11 agonistic anti-Fa

152 Treatment of HT29 cells with mitomycin C resulted in the dose-depende

153 Blocking cdc25A expression in HT29 cells with small interfering RNA attenuated FdUrd-i

154 During hypoxic conditions, treatment of HT29 cells with the AR inhibitor fidarestat significantl

155 Treatment of HT29 cells with the Src inhibitor PP2, expression of a k

156 h TLR3 and TLR4 was enhanced by treatment of HT29 cells with their respective ligands.

157 pe for 24 hr before FdUrd treatment provided HT29 cells with virtually complete protection from cytot

158 Transfection of HT29 cells with wild-type and mutated promoter/enhancer

159 f troglitazone on POX activation, whereas in HT29 cells, with a mutant p53 and wild type PPARgamma, i

160 tly reduced migration rates of AQP1-positive HT29 cells without affecting viability.

161 n nocodazole- and serum-starved synchronized HT29 cells, without affecting the G(1)-S transition in a