Pectin modified with pH, heat or enzymes, has previously been shown to exhibit anti-cancer activity. However, the structural requirements for modified pectin bioactivity have rarely been addressed. In this study several pectin extracts representing different structural components of pectin were assessed for effects against colon cancer cells. Rhamnogalacturonan I (RGI) extracts reduced proliferation of DLD1 and HCT116 colon cancer cells in a dose- and time-dependent manner. RGI reduced ICAM1 gene expression and siRNA-mediated knockdown of ICAM1 expression decreased cell proliferation providing a potential novel mechanism for the anti-cancer activity of pectin. Structural analysis of bioactive and non-bioactive RGIs suggested that a homogalacturonan component is maybe essential for the anti-proliferative activity, furthering the understanding of the structural requirements for pectin bioactivity.

Pectins extracted from a variety of sources and modified with heat and/or pH have previously been shown to exhibit activity towards several cancer cell lines. However, the structural basis for the anti-cancer activity of modified pectin requires clarification. Sugar beet and citrus pectin extracts have been compared. Pectin extracted from sugar beet pulp only weakly affected the viability of colon cancer cells. Alkali treatment increased the anti-cancer effect of sugar beet pectin via an induction of apoptosis. Alkali treatment decreased the degree of esterification (DE) and increased the ratio of rhamnogalacturonan I (RGI) to homogalacturonan. Low DE per se did not play a significant role in the anti-cancer activity. However, the enzymatic removal of galactose and, to a lesser extent, arabinose from the pectin decreased the effect on cancer cells indicating that the neutral sugar-containing RGI regions are important for pectin bioactivity.

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This review discusses the structure of pectin, the effects of modification procedures used to prepare modified pectins, and the evidence for the bioactivity of these modified materials. It will consider the evidence for the selective binding of pectin fragments to the pro-metastatic regulatory protein galectin-3 (Gal3) and the potential effects of such binding on reducing the risks of the onset and prevention of cancer. The possible modes of uptake and transport by the body of orally consumed pectin will also be considered. In this context the uptake mechanisms for other dietary carbohydrates that show immunomodulating and anti-cancer properties, such as the β-glucans, will be discussed in terms of possible analogous behaviour for pectin. Finally the article will also consider other dietary carbohydrates that might provide a source of inhibitors for Gal3 and the possible roles of Gal3 and other members of the galectin family in cellular and tissue homeostasis that suggest potential roles for pectin-derived components in combating a range of chronic diseases.

Pectin is a constituent of the cell walls of fruits and vegetables, and provides an important source of dietary fibre, as well as being a functional ingredient in processed foods. In addition to the health benefits associated with dietary fibre, new health claims are emerging, particularly with regard to the bioactive roles for modified pectin as an anti-cancer agent. These suggest that the modification creates molecular fragments, some of which may bind to and inhibit the various actions of the pro-metastatic protein galectin-3. The evidence for such a mechanism and the nature of the bioactive fragments will be discussed.