ライフサイエンスコーパス: sulindac sulfide

1 bridge is not affected upon interacting with sulindac sulfide.

2 e substrates have different sensitivities to sulindac sulfide.

3 or the nonsteroidal anti-inflammatory drug, sulindac sulfide.

4 e first generation GSMs (R)-flurbiprofen and sulindac sulfide.

5 rs such as NS-398, nimesulide, SC-58125, and sulindac sulfide.

6 of Min/+ mice with the chemopreventive drug sulindac sulfide.

7 her Bcl-2 family members was unchanged after sulindac sulfide.

8 transformed cells and did not increase after sulindac sulfide.

9 as-transformed derivatives were treated with sulindac sulfide.

10 by the nonsteroidal anti-inflammatory drug, sulindac sulfide.

11 Sulindac sulfide (10 microm) altered the expression of 6

12 Neither sulindac sulfide (a cyclooxygenase inhibitor) nor sulind

13 Sulindac sulfide, a COX inhibitor, inhibited the growth

14 e evaluated the growth-inhibitory effects of sulindac sulfide, a COX-1 and COX-2 inhibitor; exisulind

15 n production were reversed by treatment with sulindac sulfide, a known COX inhibitor.

16 In this study, we show that sulindac sulfide acts both as a PPARgamma agonist and a

17 anti-inflammatory drug), R-flurbiprofen and sulindac sulfide, affect only Abeta and not Notch beta f

18 In this report, we demonstrate that sulindac sulfide also engaged the membrane death recepto

19 Thus, our results demonstrate that sulindac sulfide also engages the membrane DR pathway in

20 stern analysis supported the conclusion that sulindac sulfide altered the expression of these protein

21 and the nonsteroidal anti-inflammatory drug sulindac sulfide, analogous to those reported previously

22 Sulindac sulfide and 5'-DMI inhibited intracellular cycl

23 Both sulindac sulfide and ciglitazone, a defined peroxisome p

24 ical inhibitors specific for Ras activation, sulindac sulfide and farnesytranferase inhibitor I, mark

25 D/GSM activity, we determined the effects of sulindac sulfide and flurbiprofen on gamma-cleavage of a

26 not impaired by the Abeta42-lowering NSAIDs, sulindac sulfide and ibuprofen.

27 Treatment of BxPC-3 cells with sulindac sulfide and NS398 resulted in an induction of C

28 y, two nonsteroidal anti-inflammatory drugs, sulindac sulfide and NS398, produced a dose-dependent in

29 a critical role in the induction of NAG-1 by sulindac sulfide and other NSAIDs.

30 tosolic phospholipase A(2), COX-1, or COX-2, sulindac sulfide and PPARgamma agonists also inhibited t

31 Here we report that two different NSAIDs, sulindac sulfide and SC-'236 engage the death receptor 5

32 We show that sulindac sulfide and SC-'236-induced apoptosis is couple

33 We further show that sulindac sulfide and SC-'236-induced DR5 upregulation oc

34 rentially modulates the apoptotic effects of sulindac sulfide and SC-'236.

35 y, we show that sulindac and its metabolites sulindac sulfide and sulindac sulfone can also inhibit t

36 also found that the anti-inflammatory drugs sulindac sulfide and sulindac sulfone, which attenuate b

37 sis, and potentiated the apoptotic effect of sulindac sulfide and sulindac sulfone.

38 Indomethacin, sulindac sulfide, and zomepirac displaced [3H]PGD2 bindi

39 l anti-inflammatory drugs (NSAIDs) including sulindac sulfide are known to exert cancer chemopreventa

40 Expression of the sulindac sulfide arrested cells in G0/G1, but cells ente

41 Similarly, pretreatment with sulindac sulfide blocks the ability of EGF to induce ERK

42 parental cells and increased markedly after sulindac sulfide but was low in untreated ras-transforme

43 mma-Secretase cleavage of APP was altered by sulindac sulfide, but CD44 and Notch-1 were either insen

44 Sulindac sulfide, but not sulindac sulfone, inhibits cyc

45 Selective COX-2 (NS398) and nonselective (sulindac sulfide) COX inhibitors, as well as 5-fluoroura

46 Sulindac and sulindac sulfide decrease the levels of mitotic cyclins,

47 hysiological pattern (high Abeta40); and (4) sulindac sulfide directly and preferentially decreases A

48 We find that sulindac sulfide does not induce drastic architectural c

49 and evaluated a series of (E)-2'-des-methyl-sulindac sulfide (E-DMSS) analogues for inhibition of CO

50 Recent evidence suggests that sulindac sulfide engages the mitochondrial pathway invol

51 he novel-type 5-LO inhibitors licofelone and sulindac sulfide exhibited higher potencies in human blo

52 studies showed synergistic interactions for sulindac sulfide, exisulind, and NDGA with paclitaxel, c

53 Sulindac sulfide had little effect on COX-2 in this mode

54 The NSAIDs indomethacin and sulindac sulfide have been shown to induce apoptosis of

55 anti-inflammatory drugs (R)-flurbiprofen and sulindac sulfide, have been suggested to modulate the Al

56 conclusion, this is the first report showing sulindac sulfide, independent of cyclooxygenase, altered

57 report, we demonstrate that indomethacin and sulindac sulfide induce apoptosis of human leukemic Jurk

58 ion of PPARgamma, as well as ciglitazone and sulindac sulfide induced expression of E-cadherin, which

59 lls, but Apo2L/TRAIL efficiently potentiates sulindac sulfide-induced apoptosis as well as activation

60 ligand, the ligand for DR5, also potentiated sulindac sulfide-induced apoptosis in all of the cell li

61 als originating from the endogenous DR5, and sulindac sulfide-induced apoptosis was investigated.

62 To further delineate the role of DR5 in sulindac sulfide-induced apoptosis, we used JCA-1 prosta

63 s-associated death domain did indeed inhibit sulindac sulfide-induced apoptosis.

64 further supporting the involvement of DR5 in sulindac sulfide-induced apoptosis.

65 oduct of cyclooxygenase, only suppressed the sulindac sulfide-induced expression of two genes, with l

66 icient HCT-116 cells were more responsive to sulindac sulfide-induced gene expression than SW-480 cel

67 rmed enterocytes are relatively resistant to sulindac sulfide-induced growth inhibition and apoptosis

68 te in the G0/G1 phase of the cell cycle, and sulindac sulfide induces cell death by apoptosis.

69 Sulindac sulfide inhibited 14-3-3epsilon proteins in HT-

70 Sulindac sulfide inhibited cell growth and induced apopt

71 Sulindac sulfide inhibited PPARdelta protein expression

72 Sulindac sulfide inhibits cyclooxygenase (COX) enzyme ac

73 state NMR study demonstrating that the NSAID sulindac sulfide interacts specifically with Alzheimer d

74 Sulindac sulfide is one of the major metabolites of suli

75 bearing a single mutant Apc allele, and that sulindac sulfide may normalize enterocyte growth in thes

76 h inhibition and also dramatically inhibited sulindac sulfide-mediated p21WAF1/CIP1 upregulation.

77 st potent agent (IC50 = 0.003-0.150 microM); sulindac sulfide, NDGA, and 13-cis-retinoic acid had int

78 Further, in Bax-deficient cells, neither sulindac sulfide nor SC-'236 in combination with Apo2L/T

79 by 25%, and treatment of Min/+ animals with sulindac sulfide normalized both beta-catenin expression

80 n to the active anti-inflammatory metabolite sulindac sulfide or irreversible oxidation to sulindac s

81 Treatment of the cells with Exisulind, sulindac sulfide, OSI-461, the guanylyl cyclase activato

82 In this study we confirmed that sulindac and sulindac sulfide prevent HT-29 cells from progressing fr

83 We conclude that sulindac and sulindac sulfide reduce the levels of major components o

84 However, sulindac sulfide reduced levels of cyclin D1 protein and

85 Importantly, the concentration of sulindac sulfide required to inhibit NSCLC cell growth g

86 We have shown that sulindac and sulindac sulfide reversibly reduce the proliferation rat

87 ollectively, our results suggest that unlike sulindac sulfide, SC-'236 in combination with Apo2L/TRAI

88 Sulindac sulfide specifically up-regulated the DR5 level

89 Here, we show that the NSAID, sulindac sulfide (SS) can potently inhibit the invasion

90 For comparison, we included the compound sulindac sulfide (SS), because sulindac compounds are we

91 At micromolar concentrations, sulindac sulfide stimulated apoptosis and inhibited the

92 Furthermore, administration of sulindac sulfide to Apc1638N mice did not alter enterocy

93 nation for this finding is the metabolism of sulindac sulfide to inactive metabolites by the peroxida

94 and p21WAF1/CIP1 upregulation in response to sulindac sulfide treatment in PNT1A cells.

95 Sulindac sulfide treatment restored DR-5 expression and,

96 Sulindac sulfide up-regulated DR5 and activated the prox

97 For example, sulindac sulfide upregulates DR5 in both Bax-deficient a

98 nonsteroidal anti-inflammatory drug (NSAID) sulindac sulfide were synthesized as potential agonists

99 TID as well as two inhibitors, ibuprofen and sulindac sulfide, which bind the cyclooxygenase active s

100 To test this hypothesis sulindac sulfide, which is used to treat familial adenom