Suppression of Intestinal Polyp Development by Nimesulide, a Selective Cyclooxygenase‐2 Inhibitor, in Min Mice

Nakatsugi, Seiichi; Fukutake, Masato; Takahashi, Mami; Fukuda, Kazunori; Isoi, Takashi; Taniguchi, Yasuaki; Sügimura, Takashi; Wakabayashi, Keiji

doi:10.1111/j.1349-7006.1997.tb00337.x

Cited by 77 publications

(35 citation statements)

References 19 publications

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“…These expression level changes of COX-2, iNOS, and adipocytokines, especially iNOS, could be associated with intestinal polyp development in Min mice. Indeed, it has been reported that iNOS inhibition, Pai-1 inhibition, COX-2 inhibition, and IL-6 knock out suppressed intestinal polyp development in Min mice (31,38,39,40). It has also been reported that 100-ppm atorvastatin treatment in Min mice slightly, but not significantly, reduced the activity and expression levels of COX-2 in the intestinal polyp (20).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Teraoka

Mutoh

Takasu

et al. 2011

Cancer Prevention Research

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It has been suggested that hyperlipidemia is positively associated with colon carcinogenesis. Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors, reduce serum lipid levels. In this study, we clarified the effects of a novel chemically synthesized statin, pitavastatin, on intestinal polyp formation in Min mice, and further examined serum lipid and adipocytokine levels, and proinflammatory and adipocytokine gene levels in intestinal mucosa of Min mice. Treatment with pitavastatin at doses of 20 and 40 ppm decreased the total number of polyps dose-dependently to 85.2% and 65.8% (P < 0.05) of the untreated value, respectively. Serum levels of total cholesterol and triglyceride were slightly reduced and those of IL-6, leptin, and MCP-1 were decreased by 40-ppm pitavastatin treatment. mRNA expression levels of cyclooxygenase-2, IL-6, inducible nitric oxide (iNOS), MCP-1, and Pai-1 were significantly reduced in intestinal nonpolyp parts by pitavastatin treatment. Among them, iNOS mRNA levels were also reduced in the intestinal polyps. Moreover, oxidative stress represented by 8-nitroguanosine in the small intestinal epithelial cells was reduced by pitavastatin treatment. Related to these proinflammatory genes, PPARg activity was activated in the intestinal nonpolyp parts and in the liver of Min mice with pitavastatin treatment. These results indicated that pitavastatin has potential benefit for the suppression of intestinal polyp development. Cancer Prev Res; 4(3); 445-53. Ó2011 AACR.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Teraoka

Mutoh

Takasu

et al. 2011

Cancer Prevention Research

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“…34,35) We have also found an increase of cytokines and arachidonic acid cascade-related enzymes, phospholipase A 2 and COX-2, in rat colon carcinogenesis. 36 39) However, the mechanism by which COX-2 inhibitors suppress carcinogenesis is not clear.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Nabumetone, a Cyclooxygenase‐2 Inhibitor, and Esculetin, a Lipoxygenase Inhibitor, on N‐Methyl‐N‐nitrosourea‐induced Mammary Carcinogenesis in Rats

Matsunaga

Yoshimi²,

Yamada³

et al. 1998

Japanese Journal of Cancer Research

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We investigated the modifying effects of nabumetone, a relatively selective cyclooxygenase-2 inhibitor, and esculetin, a lipoxygenase inhibitor, on N-methyl-N-nitrosourea(MNU)-induced mammary carcinogenesis in female Sprague-Dawley rats. A total of 124 rats, 6 weeks old, were divided into 6 groups. At 50 days of age, groups 1, 2, and 3 were treated with MNU (50 mg/kg body weight) by subcutaneous injection. From the age of 8 weeks, groups 2 and 4 were given 0.03% nabumetone in the diet and groups 3 and 5 were given 0.03% esculetin in the diet. All rats were necropsied at the termination (25 weeks after the start of experiment). The incidence and multiplicity of neoplasms in group 2 were significantly smaller than those in group 1 (P< < < <0.005 and P< < < <0.001, respectively).The incidence of neoplasms in group 3 was also significantly smaller than that in group 1 (P< < < <0.05). These results indicate that the intake of nabumetone or esculetin during the time corresponding to the post initiation phase has a chemopreventive effect on MNU-induced mammary carcinogenesis in rats.

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“…A consistent finding has been that tumour incidence and multiplicity are reduced by both nonselective NSAIDs (Reddy et al 1993, Rao et al 1995, Boolbol et al 1996, Jacoby et al 1996, and selective COX-2 inhibitors (Table 3). In addition, those tumours that do develop in drug-treated animals tend to be reduced in size relative to those in control animals (Nakatsugi et al 1997, Fukutake et al 1998, Jacoby et al 2000a,b, Reddy et al 2000a. It is notable that selective COX-2 inhibitors appear to be at least as effective in preventing tumours as nonselective NSAIDs.…”

Section: Pharmacological Studies In Rodent Models Of Intestinal Tumormentioning

confidence: 99%

Cyclooxygenase-2: a target for the prevention and treatment of breast cancer.

Howe

Subbaramaiah

Brown

et al. 2001

Endocrine-Related Cancer

292

218

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Cyclooxygenase-2 (COX-2), an inducible prostaglandin synthase, is normally expressed in parts of the kidney and brain. Aberrant COX-2 expression was first reported in colorectal carcinomas and adenomas, and has now been detected in various human cancers, including those of the breast. Strikingly, COX-2 overexpression in murine mammary gland is sufficient to cause tumour formation. To date, the role of COX-2 in tumorigenesis has been most intensively studied in the colon. Thus, the relationship between COX-2 and neoplasia can best be illustrated with reference to intestinal tumorigenesis. Here we consider the potential utility of selective COX-2 inhibitors for the prevention and treatment of breast cancer. Data for cancers of the colon and breast are compared where possible. In addition, the mechanisms by which COX-2 is upregulated in cancers and contributes to tumorigenesis are discussed. Importantly, several recent studies of mammary tumorigenesis in animal models have found selective COX-2 inhibitors to be effective in the prevention and treatment of breast cancer. Clinical trials will be needed to determine whether COX-2 inhibition represents a useful approach to preventing or treating human breast cancer.

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Suppression of Intestinal Polyp Development by Nimesulide, a Selective Cyclooxygenase‐2 Inhibitor, in Min Mice

Cited by 77 publications

References 19 publications

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Inhibitory Effects of Nabumetone, a Cyclooxygenase‐2 Inhibitor, and Esculetin, a Lipoxygenase Inhibitor, on N‐Methyl‐N‐nitrosourea‐induced Mammary Carcinogenesis in Rats

Cyclooxygenase-2: a target for the prevention and treatment of breast cancer.

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