Phytochemicals have long been effective partners in the fight against several diseases, including cancer. Among these, flavonoids are valuable allies for both cancer prevention and therapy since they are known to influence a large panel of tumor-related processes. Particularly, it was revealed that quercetin, one of the most common flavonoids, controls apoptosis and inhibits migration and proliferation, events essential for the development of cancer. In this review, we collected the evidence on the anti-cancer activity of quercetin exploring the network of interactions between this flavonol and the proteins responsible for cancer onset and progression focusing on breast, colorectal and liver cancers, owing to their high worldwide incidence. Moreover, quercetin proved to be also a potentiating agent able to push further the anti-cancer activity of common employed anti-neoplastic agents, thus allowing to lower their dosages and, above all, to sensitize again resistant cancer cells. Finally, novel approaches to delivery systems can enhance quercetin's pharmacokinetics, thus boosting its great potentiality even further. Overall, quercetin has a lot of promise, given its multi-target potentiality; thus, more research is strongly encouraged to properly define its pharmaco-toxicological profile and evaluate its potential for usage in adjuvant and chemoprevention therapy.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9918234PMC
http://dx.doi.org/10.3390/ijms24032952DOI Listing

Publication Analysis

Top Keywords

anti-cancer activity
12
activity quercetin
8
breast colorectal
8
colorectal liver
8
quercetin
5
cancer
5
targets involved
4
involved anti-cancer
4
quercetin breast
4
liver neoplasms
4

Similar Publications

Phytoplankton plays a crucial role in the fate of pollutants in aquatic ecosystems by biotransformation and bioaccumulation. Aniline was listed in priority pollutants due to its toxicity and widespread distribution in the aquatic environment. This study focused on investigating the capacity and mechanism of eukaryotic alga Chlamydomonas reinhardtii in transforming aniline.

View Article and Find Full Text PDF

Effective cancer therapies must address the tumor microenvironment (TME), a complex network of tumor cells and stromal components, including endothelial, immune, and mesenchymal cells. Durable outcomes require targeting both tumor cells and the TME while minimizing systemic toxicity. Interleukin-2 (IL-2)-based therapies have shown efficacy in cancers such as metastatic melanoma and renal cell carcinoma but are limited by severe side effects.

View Article and Find Full Text PDF

The present research aimed to assess the anti-cancer effects of the polysaccharide fraction (SJP) isolated from . The release of immune-activating cytokines, including IL-6, IL-12, and TNF-α, was markedly stimulated by the SJP in a concentration-dependent manner within the range of 1 to 100 µg/mL. Furthermore, the prophylactic intravenous () and per os () injection of SJP boosted the cytolytic activity mediated by NK cells and CTLs against tumor cells.

View Article and Find Full Text PDF

Polydatin-Induced Shift of Redox Balance and Its Anti-Cancer Impact on Human Osteosarcoma Cells.

Curr Issues Mol Biol

December 2024

Department of Clinical Sciences and Translational Medicine, University of Rome 'Tor Vergata', Via Montpellier 1, 00133 Rome, Italy.

Cancer cells demonstrate remarkable resilience by adapting to oxidative stress and undergoing metabolic reprogramming, making oxidative stress a critical target for cancer therapy. This study explores, for the first time, the redox-dependent anticancer effects of Polydatin (PD), a glucoside derivative of resveratrol, on the human Osteosarcoma (OS) cells SAOS-2 and U2OS. Using cell-based biochemical assays, we found that cytotoxic doses of PD (100-200 µM) promote ROS production, deplete glutathione (GSH), and elevate levels of both total iron and intracellular malondialdehyde (MDA), which are key markers of ferroptosis.

View Article and Find Full Text PDF

GV1001, hTERT Peptide Fragment, Prevents Doxorubicin-Induced Endothelial-to-Mesenchymal Transition in Human Endothelial Cells and Atherosclerosis in Mice.

Cells

January 2025

The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, University of California, 714 Tiverton Ave, Los Angeles, CA 90095, USA.

Doxorubicin is a highly effective anticancer agent, but its clinical use is restricted by severe side effects, including atherosclerosis and cardiomyopathy. These complications are partly attributed to doxorubicin's ability to induce endothelial-to-mesenchymal transition (EndMT) in vascular endothelial cells, a critical process in the initiation and progression of atherosclerosis and cardiomyopathy. GV1001, a multifunctional peptide with anti-inflammatory, anti-cancer, antioxidant, and anti-Alzheimer's properties, has demonstrated inhibition of EndMT.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!