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Aquamin and Prevention of Colon Cancer

ABSTRACT: In the proposed study, investigators will conduct a 90-day dietary intervention study in human subjects. Thirty individuals at risk for adenomatous colon polyp formation will be randomized to receive a calcium and multi-mineral-rich natural product (Aquamin) or a comparable level of calcium alone. There will also be a placebo group. Prior to ingesting the study agents and following the course of treatment, colonic biopsies will be obtained by sigmoidoscopy and quantitatively examined for markers of growth and differentiation. In this study, metabolomic and microbial profiles will also be generated from fecal and colon mucosal samples taken at baseline and study endpoint.

DISEASE(S): Colonic Cancer,Colorectal Cancer,Colonic Neoplasms

PROVIDER: 2205605 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description:Background. Recent studies demonstrated that Aquamin®, a calcium-, magnesium-, and multiple trace element-rich natural product, improves barrier structure and function in colonoids obtained from the tissue of healthy subjects. The goal of the present study was to determine if the colonic barrier could be improved in tissue from subjects with ulcerative colitis (UC). Methods. Colonoid cultures were established with colon biopsies from 9 individuals with UC. The colonoids were then incubated for a 2-week period under control conditions (i.e., in culture medium with a final calcium concentration of 0.25 mM) or in the same medium supplemented with Aquamin® to provide 1.5 – 4.5 mM calcium. Effects on differentiation and barrier improvement were determined using several approaches: phase-contrast & scanning electron microscopy, quantitative histology & immunohistology, mass spectrometry-based proteome assessment and transmission electron microscopy. Results. While there were no gross changes in colonoid appearance, there was evidence of increased differentiation (larger lumen diameter and wall thickness) and greater expression of cytokeratin 20 (CK20) and lesser expression of Ki67 with the intervention. Aquamin®-treated colonoids demonstrated a modest up-regulation of tight junctional proteins but stronger induction of adherens junction proteins and desmosomal proteins. Increased desmosomes were seen at the ultrastructural level. Proteomic analysis also demonstrated increased expression of basement membrane proteins and hemidesmosomal components. Proteins expressed at the apical surface (mucins and trefoils) were also increased as were several additional proteins with anti-microbial activity or that modulate inflammation. Similarly, growth and cell cycle regulatory proteins (e.g., Ki67, nucleophosmin, and stathmin) were significantly down-regulated. Laminin interactions, fibronectin matrix formation and extracellular matrix organization were the top three up-regulated pathways with the intervention. Conclusion. A majority of individuals including patients with UC do not reach the recommended daily intake for calcium and other minerals. To the extent that such deficiencies might contribute to the weakening of the colonic barrier, the findings employing UC tissue-derived colonoids here suggest that adequate mineral intake might improve the colonic barrier

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Aquamin and Prevention of Colon Cancer

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