Dietary Lifestyle and Colorectal Cancer Onset, Recurrence, and Survival: Myth or Reality?

Lofano, Katia; Principi, Mariabeatrice; Scavo, Maria Principia; Pricci, Maria; Ierardi, Enzo; Leo, Alfredo Di

doi:10.1007/s12029-012-9425-y

Cited by 29 publications

(23 citation statements)

References 98 publications

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“…Maintaining a healthy weight and keeping red meat intake to a minimum have been correlated to decreased CRC risk [13,17]. This relationship between diet and cancer has been an area of extensive research.…”

Section: The Unmet Clinical Need For Colorectal Cancer Preventionmentioning

confidence: 99%

“…This relationship between diet and cancer has been an area of extensive research. Dietary intake of certain vitamins such as calcium and folic acid, fiber, antioxidants, and phytochemicals, including curcumin and resveratrol, has been implicated in protection against CRC [17,18]. Despite this work, the exact mechanisms by which obesity predisposes to CRC, and interventions to counteract these risks, remain elusive.…”

Section: The Unmet Clinical Need For Colorectal Cancer Preventionmentioning

confidence: 99%

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Translating colorectal cancer prevention through the guanylyl cyclase C signaling axis

Blomain

Lin

Kraft

et al. 2013

Expert Review of Clinical Pharmacology

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Summary Colorectal cancer is a major public health concern, ranking among the leading causes of cancer death in both men and women. Because of this continued burden there is a clear need for improved treatment, and more importantly prevention, of this disease. In recent years there is significant evidence to support the hypothesis that guanylyl cyclase C (GUCY2C) is a tumor suppressor in the intestine, and that the loss of hormone ligands for this receptor is an important step in the disease process. Thus, ligand replacement therapy has been proposed as a strategy to prevent colorectal cancer. Until recently this strategy was not clinically plausible; however, the recent regulatory approval of Linaclotide (LINZESS™, Forest Laboratories and Ironwood Pharmaceuticals, Inc.), an oral GUCY2C ligand, has raised the possibility of utilizing this strategy clinically to prevent colorectal cancer.

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Section: The Unmet Clinical Need For Colorectal Cancer Preventionmentioning

confidence: 99%

Section: The Unmet Clinical Need For Colorectal Cancer Preventionmentioning

confidence: 99%

Translating colorectal cancer prevention through the guanylyl cyclase C signaling axis

Blomain

Lin

Kraft

et al. 2013

Expert Review of Clinical Pharmacology

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“…Studies indicate that diet and lifestyle choices play a significant role in the development of and prognosis of colon cancer (2). Vitamin D status of an individual is also influenced by both diet and lifestyle (3).…”

Section: Introductionmentioning

confidence: 99%

Increased Dietary Vitamin D Suppresses MAPK Signaling, Colitis, and Colon Cancer

et al. 2014

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Epidemiologic studies associate low serum vitamin D levels with an increased risk of colon cancer and inflammatory diseases such as inflammatory bowel disease (IBD). 129-Smad3tm1Par/J (Smad3−/−) mice are a model of bacterial-driven colitis and colon cancer when infected with Helicobacter bilis. Thus, we used this mouse model to determine whether increased dietary vitamin D would reduce inflammation and colon cancer. Smad3−/− mice were fed purified diet with either maintenance (1 IU vitamin D/g diet; maintenance) or increased concentrations of vitamin D (5 IU vitamin D/g diet; high vitamin D). One week after diet initiation, mice were inoculated with broth or H. bilis and were necropsied at several time points post-inoculation to assess inflammation, dysplasia, and neoplasia incidence. At 16 weeks post infection, 11% of mice fed high vitamin D diet had cancer compared to 41% of mice fed maintenance diet (p=0.0121). Evaluation at an early time point (1 week post-infection) showed that animals fed high vitamin D had decreased MAPK (p-p38 and p-JNK) activation in lamina propria leukocytes as well as decreased NFκB activation in colonic epithelial cells. Reduction in MAPK and NFκB activation correlated with decreased IBD scores (2.7 vs 15.5, p<0.0001) as well as decreased inflammatory cell infiltrates and reduced expression of proinflammatory cytokines in cecal tissue. These findings suggest that increased dietary vitamin D is beneficial in preventing inflammation-associated colon cancer through suppression of inflammatory responses during initiation of neoplasia or early stage carcinogenesis.

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“…Epidemiological studies demonstrate an inverse correlation between calcium intake and the risk of colorectal tumor development . In the colon, the calcium‐sensing receptor (CaSR) is a tumor suppressor that mediates, at least in part, the antiproliferative and prodifferentiating actions of calcium .…”

mentioning

confidence: 99%

miR-135b- and miR-146b-dependent silencing of calcium-sensing receptor expression in colorectal tumors

et al. 2015

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Studies have shown that the calcium‐sensing receptor (CaSR) mediates the antitumorigenic effects of calcium against colorectal cancer (CRC). Expression of the CaSR in colorectal tumors is often reduced. We have reported previously that silencing of CaSR in CRC is caused in part by methylation of CaSR promoter 2 and loss of histone acetylation. We investigated the impact of aberrant microRNA expression on loss of CaSR expression. A microarray study in two Caco‐2 subclones (Caco2/AQ and Caco2/15) that have similar genetic background, but different CaSR expression levels (Caco2/AQ expressing more CaSR than Caco2/15), identified 22 differentially expressed microRNAs that potentially target the CaSR. We validated these results by performing gain‐ and loss‐of‐function studies with the top candidates: miR‐9, miR‐27a, miR‐135b, and miR‐146b. Modulation of miR‐135b or miR‐146b expression by mimicking or inhibiting their expression regulated CaSR protein levels in two different colon cancer cell lines: Caco2/AQ (moderate endogenous CaSR expression) and HT29 (low endogenous CaSR levels). Inhibition of miR‐135b and miR‐146b expression led to high CaSR levels and significantly reduced proliferation. In samples of colorectal tumors we observed overexpression of miR‐135b and miR‐146b, and this correlated inversely with CaSR expression (miR‐135b: r = −0.684, p < 0.001 and miR‐146b: r = −0.448, p < 0.001), supporting our in vitro findings. We demonstrate that miR‐135b and miR‐146b target the CaSR and reduce its expression in colorectal tumors, reducing the antiproliferative and prodifferentiating actions of calcium. This provides a new approach for finding means to prevent CaSR loss, developing better treatment strategies for CRC.

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Dietary Lifestyle and Colorectal Cancer Onset, Recurrence, and Survival: Myth or Reality?

Cited by 29 publications

References 98 publications

Translating colorectal cancer prevention through the guanylyl cyclase C signaling axis

Translating colorectal cancer prevention through the guanylyl cyclase C signaling axis

Increased Dietary Vitamin D Suppresses MAPK Signaling, Colitis, and Colon Cancer

miR-135b- and miR-146b-dependent silencing of calcium-sensing receptor expression in colorectal tumors

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