Lectins are substantially destroyed by overnight soaking and pressure-cooking for as little as 15 minutes. But do they offer benefits, especially in cancer prevention? This seems important because many otherwise healthy foods contain lectins, and avoidable cancer mortality concerns everyone.
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Lectins have potential as oral drugs since they are often resistant to digestion. Importantly they survive passage through the gut, bind to gastrointestinal cells, enter the circulation intact, and maintain their biological activity [7]. Plant lectins from nuts and seeds are the most widely studied, especially Concanavalin A (ConA), a homo-tetramer (4 × 26.5 kDa) with Mn(II) and Ca(II) ions bound at 4 binuclear binding sites per tetramer, and with specificity for mannosyl and glycosyl sugars [8,9]. Interestingly, despite the high similarity amongst plant lectins, many have shown remarkably distinct biological profiles, with a vast range of biological activities which include anti-inflammatory [10], antidepressive [11], anticonceptive [12] and vasodilatory activities [8]. A few lectins have been recently identified as promising antitumour agents, for example ConA and the lectin ML-I from mistletoe are in pre-clinical and clinical trials for human liver cancer and malignant melanoma [13,14].
Lectins appear to inhibit tumour growth in vitro and in vivo by preferential binding to cell membranes of cancer cells or to their receptors [7,15,16]. Nevertheless, this binding leads to different cellular effects that depend on the lectin, such as the activation of protein kinases, or alteration of the production of interleukins leading to immunological responses [7]. Additionally, plant lectins also have a role in triggering different cell death pathways, including apoptosis, necrosis and/or autophagy [3,7,14,17–19]. For example, ML-I (Mistletoe lectin I from Viscum album) and Ricin A (from Ricinus communis) bind to ribosomes and inhibit protein synthesis in vitro, while RBA (Rice bran agglutinin) or WGA (Wheat germ agglutinin) induce G2/M cell cycle arrest and downstream apoptosis [7]. BFL (from Bauhinia forficata) has potent anticancer activity towards MCF-7 cancer cells, causing DNA fragmentation and cell cycle arrest at the G2/M phase, along with inhibition of caspase 9 leading to primary and secondary necrosis [20]. However, determination of their mechanism of action is not always straightforward. Another similar lectin BG2 (from Bauhinia variegata) inhibits cell proliferation of MCF-7 breast cancer cells and HepG2 hepatomas