ライフサイエンスコーパス: HCT-116 cell

1 fectively induced necrotic cell death in the HCT 116 cells.

2 ectal cancer cell lines, including HT-29 and HCT 116 cells.

3 is required for TRAIL-mediated apoptosis in HCT 116 cells.

4 CT 116-R30A cells was 15% of that present in HCT 116 cells.

5 a subline derived from mitomycin C-sensitive HCT 116 cells.

6 risk SNP of colorectal cancer, rs6983267, in HCT-116 cells.

7 otent cytotoxic effect in Caco-2 compared to HCT-116 cells.

8 sin expression increased colony formation by HCT-116 cells.

9 rable uptake and subcellular localization in HCT-116 cells.

10 apoptosis was also investigated in HT-29 and HCT-116 cells.

11 o induce toxicity and apoptosis in HT-29 and HCT-116 cells.

12 c-tagged CUGBP2 colocalize in the nucleus of HCT-116 cells.

13 -2 overexpression in Saos-2 cells but not in HCT-116 cells.

14 RNA suppressed LY294002-induced apoptosis in HCT-116 cells.

15 le proteins and did not induce caveolin-1 in HCT-116 cells.

16 tosis, cell cycle, and cell growth arrest in HCT-116 cells.

17 sequently, enhanced the survival of p53(-/-) HCT-116 cells.

18 riety of nonfarnesylated substrates of FT in HCT-116 cells.

19 cumin-induced G(2)/M arrest and apoptosis in HCT-116 cells.

20 ting in G(2)/M phase arrest and apoptosis in HCT-116 cells.

21 s a pivotal role in TGZ-induced apoptosis in HCT-116 cells.

22 ecrease in promoter activity was observed in HCT-116 cells.

23 c nude mice compared with vector-transfected HCT-116 cells.

24 to increased clonogenicity of HCA-7, but not HCT-116 cells.

25 eater CDDP and HN2-sensitivity than parental HCT-116 cells.

26 ies identified actin as a putative target in HCT-116 cells, a result that was validated by mass spect

27 Inhibition of ERK phosphorylation in HCT-116 cells abolishes the Egr-1 induction by TGZ, sugg

28 The ATR(+/-) HCT 116 cells also displayed compromised activation of C

29 Microarray analyses of untreated HCT 116 cells and those exposed to either 1 (1 micromol/

30 (control) and 60 (100 micro M celecoxib) in HCT-116 cells and 22 (control) and 36 (100 micro M celec

31 he gene expression profiles of wild-type p53 HCT-116 cells and an isogenic p53 knockout counterpart a

32 Treatment of human colorectal cancer HCT-116 cells and human prostate cancer PC-3 cells, but

33 s regulated by PI3K/AKT/GSK-3beta pathway in HCT-116 cells and may provide a further understanding of

34 Studies were performed in human colon cancer HCT-116 cells and murine embryonic fibroblasts (MEF) wit

35 ug-activated gene-1 (NAG-1) and apoptosis in HCT-116 cells, and in time-course studies, the PPARgamma

36 cells to CDDP and HN2 was not limited to the HCT-116 cell background since MEF from p21 knockout mice

37 was hypomethylated and activated in DNMT1-/- HCT 116 cells but not in DNMT3B null cells, indicating a

38 oxazolidine fails to induce a G2/M arrest in HCT-116 cells but induces apoptosis 4-fold better than d

39 vely kill p53 wild-type colorectal carcinoma HCT-116 cells but not p53 null cells.

40 he controls and in the presence of PGA(1) in HCT-116 cells but were 22 and 4, respectively, in HT-29

41 ) < 1 nM vs human colorectal adenocarcinoma (HCT-116) cells) but did not exhibit microfilament-disrup

42 ing enhanced the association of liposomes to HCT 116 cells by almost 5-fold.

43 the activities observed using MDA-MB-231 and HCT-116 cell-conditioned medium after transfection with

44 CD19(+) B cells from IBD patients induced HCT-116 cell death.

45 the probe with commercial Lysotracker Red in HCT 116 cells demonstrated the specific localization of

46 itory activity in vitro (GI50 < 1muM against HCT-116 cells), demonstrating 3- to 10-fold greater pote

47 sion of TRAIL increased DNA fragmentation of HCT-116 cells, demonstrating the functional activity of

48 Analysis of genomic DNA from HCT-116 cells determined that these cells possess aberra

49 that displayed by normal human fibroblasts, HCT-116 cells display moderate radiosensitivity compared

50 In HCT-116 cells, exogenously added 15-LO-1 metabolites, 13

51 In contrast, the clonogenic survival of HCT-116 cells exposed to ionizing radiation, adriamycin,

52 As HCT-116 cells express autocrine PG, the in situ associat

53 In HCT-116 cells expressing the Glu-125 TK mutant, GCV meta

54 HCT-116 cells had the lowest level (0.2%) of guanine bei

55 ent by restriction enzyme MspI revealed that HCT 116 cells have two heterozygous NQO1 alleles, a wild

56 d suppressed growth of xenograft tumors from HCT-116 cells in nude mice.

57 ound 1 exhibited potent cytotoxicity against HCT-116 cells in vitro.

58 fluorescence microscopy imaging of COS-7 and HCT 116 cells incubated with probe I showed endosomal se

59 n vitro(99m)Tc-HYNIC-TCP-1 binding assays on HCT 116 cells indicated a mean Kd of 3.04+/-0.52nM.

60 hat bile acid-induced apoptosis in HT-29 and HCT-116 cells is enantiospecific, hence correlated with

61 gh miR-145 inhibits cell growth in MCF-7 and HCT-116 cells, it has no significant effect on cell grow

62 For comparison, HCT-116 cells lacking p53 function were also prepared th

63 e of this enhanced sensitivity revealed that HCT-116 cells lacking p53 or p21 function exhibited a re

64 To further study the mechanism, we cultured HCT 116 cell line in vitro.

65 However, in the human colon carcinoma HCT-116 cell line, which is deficient in COX-2, retrovir

66 aspases was also more pronounced in DLD1 and HCT 116 cell lines.

67 gene candidates induced apoptosis in stable HCT 116 cell lines.

68 Apoptosis analysis in U87-MG and HCT-116 cell lines suggested that these compounds delaye

69 nds against MCF-7, HCT-116, and p53 knockout HCT-116 cell lines.

70 epithelial (IEC-18) and human colon cancer (HCT-116) cell lines were generated.

71 he overexpression of wild-type p53 gene into HCT-116 cells mimicked the effect of MNNG-induced expres

72 In the HCT-116 cells, NAG-1 expression is increased and apoptos

73 However, this response was diminished in HCT-116 cells overexpressing cyclooxygenase-1 compared w

74 ion fifty (IC50) for BL, SH, RG on HT-29 and HCT-116 cell proliferation ranged 0.9-2.0mg/mL.

75 Irradiation of HCT-116 cells resulted in phosphorylation of AKT that wa

76 108NF micelles, and subsequent incubation in HCT 116 cells, resulted in very high lysosomal colocaliz

77 ntable tumors derived from NAG-1 transfected HCT-116 cells showed reduced tumorigenicity in athymic n

78 Proliferation assays using HCT-116 cells showed that addition of inhibitors phenyla

79 Inhibition of miR-451a in HCT-116 cells significantly decreased cell proliferation

80 essing cyclooxygenase-1 compared with normal HCT-116 cells suggesting the presence of cyclooxygenase

81 Neurotensin activated Akt in HCT-116 cells; this effect was inhibited by blocking miR

82 e show that hMLH1 complementation sensitizes HCT 116 cells to methylseleninic acid, methylselenocyste

83 lfonium salts that produced a pH drop within HCT 116 cells via the generation of a photoacid within t

84 tivation of beta-catenin in curcumin-treated HCT-116 cells was unpreventable by caspase-3 inhibitor Z

85 In HCT 116 cells, we found two mRNAs coding full-length cDN

86 Colon carcinoma HCT 116 cells were cultured and grown into three-dimensi

87 Cyclooxygenase-deficient HCT-116 cells were more responsive to sulindac sulfide-i

88 nt of R2 in response to DNA damage, p53(-/-) HCT-116 cells were stably transfected with an expression

89 ws potent antiproliferative activity against HCT-116 cells, whereas arenimycins C (2) and D (3) displ

90 h levels of COX-2 protein constitutively and HCT-116 cells which lack COX-2 protein.

91 urthermore, in stable overexpressing 15-LO-1 HCT-116 cells, which produce endogenous 15-LO-1 metaboli

92 endently of p53 in isogenic pairs of RKO and HCT 116 cells with differential p53 status.

93 K1 protein expression following treatment of HCT 116 cells with growth inhibitory concentrations of 1

94 lorectal cancer cells and the MMR-proficient HCT 116 cells with hMLH1 complementation to investigate

95 Pretreatment of the hMLH1-complemented HCT 116 cells with the antioxidant N-acetylcysteine or 2

96 Transfection of HCT-116 cells with a constitutively active AKT reduced a

97 HCT-116 cells with disrupted p21 genes also exhibited gr

98 53 and NQO1 was not affected by treatment of HCT-116 cells with ES936, demonstrating that the associa

99 scored by our observations that co-culturing HCT-116 cells with the DNA demethylating agent 5-azacyti

100 cytotoxicity against human colon carcinoma (HCT-116) cells with IC(50) values between 2.1 and 4.0 mi