Legumes in combination with other products are the staple food for a large part of the world population, especially the low-income fragment, because their seeds provide valuable amounts of carbohydrates, fiber, and proteins, and have an important composition of essential amino acids, the sulphured amino acids being the limiting ones. Furthermore, legumes also have nonnutritional compounds that may decrease the absorption of nutrients or produce toxic effects; however, it has been reported that depending on the dose, these nonnutritional compounds also have different bioactivities as antioxidant, hypolipidemic, hypoglycemic, and anticarcinogenic agents, which have been proven in scientific studies. It has been observed that in countries with a high consumption of legumes, the incidence of colorectal cancer is lower. Some studies have shown that legume seeds are an alternative chemopreventive therapy against various cancers especially colon; this was verified in various animal models of induced by azoxymethane, a colon specific carcinogenic compound, in which a diet was supplemented with different concentrations of beans, lentils, chickpeas, or soybeans, mostly. These studies have proven the anticancer activity of legumes in early stages of carcinogenesis. Therefore, it is important to review the information available to elucidate the chemopreventive mechanisms of action of legume compounds.

Objective: Colon cancer occupies the third place in incidence worldwide; eating habits, in particular, consumption of hypercaloric diets, are relevant in its etiopathogenesis. On the other hand, foods can also modulate carcinogenesis: for example, proteins, which when hydrolyzed release peptides with biological activities, and legumes, especially, chickpea, represent a good source of hydrolysates. The objective of this work was to verify the inhibitory effect of chickpea hydrolyzed protein on azoxymethane (AOM)-induced carcinogenesis in mice fed a hypercaloric diet. Methods: We hydrolyzed chickpea protein by pepsin, pancreatin, and a combined pepsin–pancreatin system, to test its anticarcinogenic and hypercaloric activity in mice that had consumed a hypercaloric diet or a normal diet but were injected with azoxymethane (AOM). Results: A concentrate (70% proteins) was obtained from chickpea seeds (18.5% proteins), and extensive hydrolysates were obtained at 15 minutes, in all tested enzyme systems. The greatest activity was evidenced in the hydrolysates obtained with pepsin–pancreatin at 90 minutes. Animals that consumed the hypercaloric diet had a higher concentration of cholesterol and a higher atherogenic index, which were significantly reduced with the administration of chickpea protein hydrolysates with a dose-response effect (10, 20, or 30 mg/kg), whereas no effect was observed in animals that consumed the normal diet. In animals given AOM, aberrant crypts were observed, at a higher rate in animals that consumed the hypercaloric diet; with the consumption of hydrolysates by the animals that consumed either diet, the number of aberrant crypts was reduced with the 3 doses tested, and the effect was better in those animals fed the hypercaloric diet. The best effect in all tests was with 30 mg/kg body weight. Conclusion: The consumption of chickpea protein hydrolysates might confer a protective effect against colon carcinogenesis.

Scope: The objective of the study was to evaluate the effect of daily consumption of cooked chickpea (2% and 10%) in ICR male mice in which colon cancer was induced with azoxymethane and dextran sulfate sodium. Methods and Results: The effect of consumption of 2% or 10% cooked chickpeas on carcinogenesis-induced colon azoxymethane (AOM)/dextran sulfate sodium (DSS) in ICR mice was determined. Protein oxidation and lipids were determined by colorimetric methods and oxidation of DNA through the identification of adducts 8-hydroxy-2′-desoxiguanosine and proliferation markers (proliferating cell nuclear antigen [PCNA], Ki-67, and β-catenin), and inflammation (cyclooxygenase [COX]-2 and inducible nitric oxide synthase [iNOS]) were identified by immunohistochemistry reactions. The results showed the protective effect of daily consumption of rich cooked chickpeas in the carcinogenesis process, decreasing lipid, protein, and DNA oxidation and decreasing the expression of inflammatory enzymes (COX-2 and iNOS) as well as β-catenin, one of the most important oncogenic proteins in colon cancer. Animals that were fed with the 10% chickpea diet showed an inhibition in cellular proliferation (Ki-67 and PCNA expression). Conclusions: The addition of cooked chickpea seed (2% and 10%) to the daily diet is proposed as a chemopreventive agent against colon cancer.

Hepatocellular carcinoma (HCC) is a health problem worldwide due to its high mortality rate, and the tumor microenvironment (TME) plays a key role in the HCC progression. The current ineffective therapies to fight the disease still warrant the development of preventive strategies. Quercetin has been shown to have different antitumor activities; however, its effect on TME components in preneoplastic lesions has not been fully investigated yet. Here, we aimed to evaluate the effect of quercetin (10 mg/kg) on TME components during the early stages of HCC progression induced in the rat. Histopathological and immunohistochemical analyses showed that quercetin decreases the size of preneoplastic lesions, glycogen and collagen accumulation, the expression of cancer stem cells and myofibroblasts markers, and that of the transporter ATP binding cassette subfamily C member 3 (ABCC3), a marker of HCC progression and multi-drug resistance. Our results strongly suggest that quercetin has the capability to reduce key components of TME, as well as the expression of ABCC3. Thus, quercetin can be an alternative treatment for inhibiting the growth of early HCC tumors.