Curcumin's Effect on Intestinal Inflammation and Tumorigenesis in the Apc<sup><i>Min/+</i></sup>Mouse

Murphy, E. Angela; Davis, John M.; McClellan, Jamie L.; Gordon, Benjamin; Carmichael, Martin D.

doi:10.1089/jir.2010.0051

Cited by 46 publications

(35 citation statements)

References 28 publications

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“…However, wide variability exists between reported studies. The number of colonic tumors in this study was high but is comparable to that observed by others (38)(39)(40). The reasons for this variability remain in large part unexplained, but differences in housing conditions, diet composition, and microbiota may be have induced changes in the intestinal microenvironmental factors implicated in colon tumor formation (8,41,42) Carnitine plays a key role in the metabolism of fatty acids (17,22).…”

Section: Discussionsupporting

confidence: 91%

Studies on the Chemopreventive Effect of Carnitine on Tumorigenesis In Vivo, Using Two Experimental Murine Models of Colon Cancer

Dionne

Elimrani

Roy

et al. 2012

Nutrition and Cancer

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Carnitine is known for its essential role in intermediary metabolism. In vitro studies suggest that its antioxidant and anti-inflammatory properties are potentially beneficial toward cancer prevention. This study tested effects of carnitine on the development of colon cancer in vivo using 2 murine models: azoxymethane (AOM) treatment as a model of carcinogen-induced colon cancer and a genetically induced model using Apc (Min/+) mice. AOM and Apc (Min/+) mice divided into dietary groups varying in lipid content, with or without carnitine supplementation (0.08%). AOM-exposed mice on a high butterfat diet had significantly increased aberrant crypts (ACF) (9.3 ± 0.88 vs. 6.3 ± 0.65), and macroscopic tumors (3.8 ± 0.95 vs. 2.0 ± 0.25) compared to mice on a control diet. In AOM mice fed the high butterfat diet, carnitine supplementation inhibited ACF (4.9 ± 0.7 vs. 9.3 ± 0.88, P < 0.001), crypt multiciplicity (1.6 ± 0.08 vs. 1.92 ± 0.1, P < 0.01) and tumors (1.5 ± 0.38 vs. 3.8 ± 0.95, P < 0.001). Carnitine supplementation resulted in significantly increased tissue carnitine and acylcarnitine levels. Carnitine inhibited the development of precancerous lesions and macroscopic colonic tumors in AOM-treated mice. However, carnitine did not exert protective effects on intestinal tumors in Apc (Min/+) mice.

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Section: Discussionsupporting

confidence: 91%

Studies on the Chemopreventive Effect of Carnitine on Tumorigenesis In Vivo, Using Two Experimental Murine Models of Colon Cancer

Dionne

Elimrani

Roy

et al. 2012

Nutrition and Cancer

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“…Numerous studies have indicated that anticancer properties of CUR are related to enzymes such as COX-2, AMPK, MMPs, NADPH and LOX; transcription factors such as NF-κB, AP-1, β-catenin and STAT-3 and protein kinases and growth factors such as MAPK, AKT, JAK, VEGF, ERK, PKA and Bcl-2 ( Figure 8). 13,[91][92][93][94] More details are discussed later.…”

Section: Application Of Cur Liposomes On Cancermentioning

confidence: 99%

Liposomal curcumin and its application in cancer

Feng¹,

Wei²,

Lee³

et al. 2017

IJN

316

208

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Curcumin (CUR) is a yellow polyphenolic compound derived from the plant turmeric. It is widely used to treat many types of diseases, including cancers such as those of lung, cervices, prostate, breast, bone and liver. However, its effectiveness has been limited due to poor aqueous solubility, low bioavailability and rapid metabolism and systemic elimination. To solve these problems, researchers have tried to explore novel drug delivery systems such as liposomes, solid dispersion, microemulsion, micelles, nanogels and dendrimers. Among these, liposomes have been the most extensively studied. Liposomal CUR formulation has greater growth inhibitory and pro-apoptotic effects on cancer cells. This review mainly focuses on the preparation of liposomes containing CUR and its use in cancer therapy.

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“…Quantification of gene expression for macrophage phenotype [IL-12 and IL-23 (M1 macrophage phenotype), IL-13, CD206, TGF-␤, and CCL17 (M2 macrophage phenotype)], T cell markers (CD8 and Foxp3), and inflammatory mediators [IL-1␤, IL-6, TNF-␣, SOCS1 (suppressor of cytokine signaling 1)] were performed as previously described (28,29). Briefly, mucosal tissue and polyps were homogenized under liquid nitrogen with a Polytron, and total RNA was extracted by using TRIzol reagent (Invitrogen).…”

Section: Animals Apcmentioning

confidence: 99%

Linking tumor-associated macrophages, inflammation, and intestinal tumorigenesis: role of MCP-1

McClellan

Davis

Steiner

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

105

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Tumor-associated macrophages are associated with poor prognosis in certain cancers. Monocyte chemoattractant protein 1 (MCP-1) is thought to be the most important chemokine for recruitment of macrophages to the tumor microenvironment. However, its role on tumorigenesis in a genetic mouse model of colon cancer has not been explored. We examined the role of MCP-1 on tumor-associated macrophages, inflammation, and intestinal tumorigenesis. Male Apc Min/+, Apc Min/+/MCP-1−/− or wild-type mice were euthanized at 18 wk of age and intestines were analyzed for polyp burden, apoptosis, proliferation, β-catenin, macrophage number and phenotype, markers for cytotoxic T lymphocytes and regulatory T cells, and inflammatory mediators. MCP-1 deficiency decreased overall polyp number by 20% and specifically large polyp number by 45% ( P < 0.05). This was consistent with an increase in apoptotic cells ( P < 0.05), but there was no change detected in proliferation or β-catenin. MCP-1 deficiency decreased F4/80-positive cells in both the polyp tissue and surrounding intestinal tissue ( P < 0.05) as well as expression of markers associated with M1 (IL-12 and IL-23) and M2 macrophages (IL-13, CD206, TGF-β, and CCL17) ( P < 0.05). MCP-1 knockout was also associated with increased cytotoxic T lymphocytes and decreased regulatory T cells ( P < 0.05). In addition, MCP-1−/− offset the increased mRNA expression of IL-1β and IL-6 in intestinal tissue and IL-1β and TNF-α in polyp tissue ( P < 0.05), and prevented the decrease in SOCS1 expression ( P < 0.05). We demonstrate that MCP-1 is an important mediator of tumor growth and immune regulation that may serve as an important biomarker and/or therapeutic target in colon cancer.

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Curcumin's Effect on Intestinal Inflammation and Tumorigenesis in the Apc^Min/+Mouse

Cited by 46 publications

References 28 publications

Studies on the Chemopreventive Effect of Carnitine on Tumorigenesis In Vivo, Using Two Experimental Murine Models of Colon Cancer

Studies on the Chemopreventive Effect of Carnitine on Tumorigenesis In Vivo, Using Two Experimental Murine Models of Colon Cancer

Liposomal curcumin and its application in cancer

Linking tumor-associated macrophages, inflammation, and intestinal tumorigenesis: role of MCP-1

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Curcumin's Effect on Intestinal Inflammation and Tumorigenesis in the ApcMin/+Mouse

Cited by 46 publications

References 28 publications

Studies on the Chemopreventive Effect of Carnitine on Tumorigenesis In Vivo, Using Two Experimental Murine Models of Colon Cancer

Studies on the Chemopreventive Effect of Carnitine on Tumorigenesis In Vivo, Using Two Experimental Murine Models of Colon Cancer

Liposomal curcumin and its application in cancer

Linking tumor-associated macrophages, inflammation, and intestinal tumorigenesis: role of MCP-1

Contact Info

Product

Resources

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Curcumin's Effect on Intestinal Inflammation and Tumorigenesis in the Apc^Min/+Mouse