Anticancer and Immunomodulatory Benefits of Taro (Colocasia esculenta) Corms, an Underexploited Tuber Crop

Abstract

Taro corms contain valuable bioactive molecules effective against cancer and cancer-related risk factors, such as carcinogens and biological agents, several pathophysiological conditions, including oxidative stress and inflammation, while controlling metabolic dysfunctions and boosting the immunological response. Such broad effects are achieved by the taro health-influencing compounds displaying antitumoral, antimutagenic, immunomodulatory, anti-inflammatory, antioxidant, anti-hyperglycemic, and anti-hyperlipidemic activities. Taro bioactivities are attributed to the combination of tarin, taro-4-I polysaccharide, taro polysaccharides 1 and 2 (TPS-1 and TPS-2), A-1/B-2 α-amylase inhibitors, monogalactosyldiacylglycerols (MGDGs), digalactosyldiacylglycerols (DGDGs), polyphenols, and nonphenolic antioxidants. Most of these compounds have been purified and successfully challenged in vitro and in vivo, proving their involvement in the aforementioned activities. Although these health-promoting effects have been recognized since ancient times, as well as other valuable features of taro for food profit, such as hypo-allergenicity, gluten-free, and carbohydrates with medium-glycemic index, taro crop remains underexploited. The popularization of taro intake should be considered a dietary intervention strategy to be applied to improve the overall health status of the organism and as supportive therapy to manage tumorigenesis.

Keywords: COX-2 down-regulation; health-promoting compounds; metabolism modulation; resistant starch; taro dietary intervention.

Figure 1

Global distribution of taro production reproduced from FAOSTAT (http://www.fao.org/faostat/en/#data/QC). Quantitative taro production per country in 2018, repreScheme 230. tons followed by the USA, Canada, and Cyprus with production lower than 1600 tons. Uncolored countries represent production areas under 1000 ha.

Figure 2

Therapeutic potential of taro phytochemicals: Anti-carcinogenic effects of taro bioactive compounds on the non-canonical NF-κB pathway could be mediated by polyphenols. Polyphenols can mediate the suppression of NF-κB transcriptional factor resulting in the inhibition of pro-inflammatory signaling cascade, apoptosis induction, cell proliferation control, and metastasis. inhibitory kappa B kinase (IKK); vascular endothelial growth factor (VEGF); B-cell lymphoma 2 (BCL-2); B-cell lymphoma X (BCL-X); c-myelocytomatosis (C-MYC).

Figure 3

Putative targets of taro-derived components in metabolic pathways. Lipid and carbohydrate metabolisms can be modulated, mainly, by taro mucilage, arabinogalactan, monogalactosyldiacylglycerols (MGDG), digalactosyldiacylglycerols (DGDG) and A-1/B-2 proteins, which may act in conjunction to control glycemia, lipidemia, and downstream effects such as body weight, glucose tolerance, and glycosuria, hepatic function, atherogenesis, and coronary risk. Inhibition of human lanosterol synthase (hOSC) affects the cholesterol synthesis of pancreatic lipase (PL), reducing triacylglyceride hydrolysis to monoglycerides (MG) and free fatty acids (FA), down-regulation of salivary α-amylase, glucose release by α-glucosidase, glucose absorption, reduction of very low-density lipoprotein (VLDL) formation, and enhancement of muscle glucose uptake. Mucilage can entrap mutagenic/carcinogenic agents, 1,8 dinitropyrene (DNP) and heterocyclic amine 2-amino-3-methylimidazo[4,5-f] quinoline (IQ), avoiding their absorption and consequent effects. HMG-CoA—β-Hydroxy β-methylglutaryl-Coenzyme A; IDL—intermediate-density lipoprotein.

Figure 4

Hypothetical antitumoral tarin mechanism. (left-hand panel) Tarin binds to specific carbohydrate antigens, typically overexpressed in cancer cells, down-regulating COX-2 (cyclooxygenase 2) expression, culminating in decreased PGE2 (prostaglandin 2) synthesis and derepression of the antitumoral response. Tumor progression can be inhibited by inactivation of Ras–Raf or PIK3–Akt pathways and cell death by the activation of ROS-p38-p53 or caspase-dependent pathways, inducing apoptosis or autophagy, commonly described for GNA-related lectins. Red lines show already known tarin mechanisms. Dashed red lines indicate the main mechanisms reported for GNA-related lectins. PLA2—phospholipase A2; PG synthase—prostaglandin synthase; ROS—reactive oxygen species; Cyt. c—cytochrome c; EP1-4—prostaglandin E receptor 1-4; NK cells—natural killer cells. (right-hand panel) Anticancer effects may be boosted by the immunomodulatory abilities of tarin and other taro derivatives, whose effects are highlighted in green and include complement activation through alternative and classical pathways, natural killer (NK) cell activation, T cell activation to TCD4+ cells (Th1) and TCD8+ (CTLs—cytotoxic T lymphocytes) effectors, cytokines release by polysaccharide-activated macrophages and tarin-activated splenocytes, progenitor cell protection through the attenuation of cyclophosphamide (CY) cytotoxic effects and the proliferation of spleen and bone marrow cells. Red lines indicate tarin and polysaccharide effects, while the dotted red lines indicate the downstream effects that might be triggered by released cytokines. CLP—common lymphoid progenitor, CMP—common myeloid progenitor, BM—bone marrow.