Cancer is one of the leading causes of death in the world. Chemotherapy is presented as an option for treatment of this disease, however, low specificity, high resistance rates, toxicity and hypersensitivity reactions, make it necessary to search for therapeutic alternatives that increase the selectivity of treatment, reduce the side effects and enhance its antitumor potential. Natural products are accessible, inexpensive and less toxic sources; in addition, they have multiple mechanisms of action that can potentiate the outcome of chemotherapeutics. In this review, we present evidence on the beneficial effect of the interaction of dietary phytochemicals with chemotherapeutical agents for cancer treatment. This effect is generated by different mechanisms of action such as, increased tumoricidal effect via sensitization of cancer cells, reversing chemoresistance through inhibition of several targets involved in the development of drug resistance and, decreasing chemotherapy-induced toxicity in non-tumoral cells by the promotion of repair mechanisms. Studies discussed in this review will provide a solid basis for the exploration of the potential use of natural products in combination with chemotherapeutical agents, to overcome some of the difficulties that arise in the management of cancer patients.

The Wnt/β-Catenin pathway alterations present in colorectal cancer (CRC) are of special interest in the development of new therapeutic strategies to impact carcinogenesis and the progression of CRC. In this context, different polyphenols present in natural products have been reported to have modulatory effects against the Wnt pathway in CRC. In this study, we evaluate the effect of two polyphenol-rich coffee extracts and chlorogenic acid (CGA) against SW480 and HT-29 CRC cells. This involved the use of MTT and SRB techniques for cell viability; wound healing and invasion assay for the evaluation of the migration and invasion process; T cell factor (TCF) reporter plasmid for the evaluation of transciption factor (TCF) transcriptional activity; polymerase chain reaction (PCR) of target genes and confocal fluorescence microscopy for β-Catenin and E-Cadherin protein fluorescence levels; and subcellular localization. Our results showed a potential modulatory effect of the Wnt pathway on CRC cells, and we observed a reduction in the transcriptional activity of β-catenin. All the results were prominent in SW480 cells, where the Wnt pathway deregulation has more relevance and implies a constitutive activation of the signaling pathway. These results establish a starting point for the discovery of a mechanism of action associated with these effects and corroborate the anticancer potential of polyphenols present in coffee, which could be explored as chemopreventive molecules or as adjunctive therapy in CRC.

Colorectal cancer mortality rate and highly altered proteins from the Wnt/β-catenin pathway increase the scientific community’s interest in finding alternatives for prevention and treatment. This study aims to determine the biological effect of chlorogenic acid (CGA) on two colorectal cancer cell lines, HT-29 and SW480, and its interactions with β-catenin and LRP6 to elucidate a possible modulatory mechanism on the Wnt/β-catenin pathway. These effects were determined by propidium iodide and DiOC6 for mitochondrial membrane permeability, MitoTracker Red for mitochondrial ROS production, DNA content for cell distribution on cell cycle phases, and molecular docking for protein–ligand interactions and binding affinity. Here, it was found that CGA at 2000 µM significantly affects cell viability and causes DNA fragmentation in SW480 cells rather than in HT-29 cells, but in both cell lines, it induces ROS production. Additionally, CGA has similar affinity and interactions for LRP6 as niclosamide but has a higher affinity for both β-catenin sites than C2 and iCRT14. These results suggest a possible modulatory role of CGA over the Wnt/β-catenin pathway in colorectal cancer.

In the last few decades there has been a rise in the worldwide incidence of colorectal cancer which can be traced back to the influence of well-known modifiable risk factors such as lifestyle, diet and obesity. Conversely, the consumption of fruits, vegetables and fiber decreases the risk of CRC, which is why dietary polyphenols have aroused interest in recent years as potentially anti-carcinogenic compounds. One of the driving forces of colorectal carcinogenesis, in both sporadic and hereditary CRC, is the aberrant activation/regulation of the Wnt/β-catenin pathway. This review discusses reports of modulation of the Wnt/β-Catenin signaling pathway by dietary polyphenols (resveratrol, avenanthramides, epigallocatechinin, curcumin, quercetin, silibinin, genistein and mangiferin) specifically focusing on CRC, and proposes a model as to how this modulation occurs. There is potential for implementing these dietary polyphenols into preventative and therapeutic therapies for CRC as evidenced by some clinical trials that have been carried out with promising results.

Non-alcoholic fatty liver disease is characterized by disturbed lipid metabolism and increased oxidative stress. These conditions lead to the activation of different cellular response mechanisms, including senescence. Cellular senescence constitutes an important response to injury in the liver. Recent findings show that chronic oxidative stress can induce senescence, and this might be a driving mechanism for NAFLD progression, aggravating the disturbance of lipid metabolism, organelle dysfunction, pro-inflammatory response and hepatocellular damage. In this context, the modulation of cellular senescence can be beneficial to ameliorate oxidative stress-related damage during NAFLD progression. This review focuses on the role of oxidative stress and senescence in the mechanisms leading to NAFLD and discusses the possibilities to modulate senescence as a therapeutic strategy in the treatment of NAFLD.

Colorectal cancer is one of the leading death-related diseases worldwide, usually induced by a multifactorial and complex process, including genetic and epigenetic abnormalities and the impact of diet and lifestyle. In the present study, we evaluated the biological impact of two of the main coffee polyphenols, chlorogenic acid (CGA) and caffeic acid (CA), as well as two polyphenol-rich coffee extracts (green coffee extract and toasted coffee Extract) against SW480 and SW620 colorectal cancer cells. First, the total phenolic content and the antioxidant capability of the extracts were determined. Then, cytotoxicity was evaluated by MTT and SBR. Finally, a wound healing assay was performed to determine the impact on the cell migration process. The results showed a cytotoxic effect of all treatments in a time and dose-dependent manner, which decreased the viability in both cell lines at 24 h and 48 h; likewise, the migration capability of cells decreased with low doses of treatments. These results suggest the potential of coffee to modulate biological mechanisms involved in colorectal cancer development; however, more studies are required to understand the mechanistic insights of these observations.