Abstract
Epigenetics, including DNA methylation, histone modification, and noncoding RNA regulation, are physiological regulatory changes that affect gene expression without modifying the DNA sequence. Although epigenetic disorders are considered a sign of cell carcinogenesis and malignant events that affect tumor progression and drug resistance, in view of the reversible nature of epigenetic modifications, clinicians believe that associated mechanisms can be a key target for cancer prevention and treatment. In contrast, epidemiological and preclinical studies indicated that the epigenome is constantly reprogrammed by intake of natural organic compounds and the environment, suggesting the possibility of utilizing natural compounds to influence epigenetics in cancer therapy. Flavonoids, although not synthesized in the human body, can be consumed daily and are common in medicinal plants, vegetables, fruits, and tea. Recently, numerous reports provided evidence for the regulation of cancer epigenetics by flavonoids. Considering their origin in natural and food sources, few side effects, and remarkable biological activity, the epigenetic antitumor effects of flavonoids warrant further investigation. In this article, we summarized and analyzed the multi-dimensional epigenetic effects of all 6 subtypes of flavonoids (including flavonols, flavones, isoflavones, flavanones, flavanols, and anthocyanidin) in different cancer types. Additionally, our report also provides new insights and a promising direction for future research and development of flavonoids in tumor prevention and treatment via epigenetic modification, in order to realize their potential as cancer therapeutic agents.
Highlights
Cancer is a chronic consumptive disease that has not been overcome yet and has become a global health problem threatening human life [1, 2]
This study suggests that quercetin and B, in combination, can regulate abnormal epigenetic changes through the HDAC1-IR-NF-kB signaling axis and inhibit growth of the human esophageal cancer cell line Eca9706
After collecting tumors from nude mice and administering quercetin, promotion of miR-21 was associated with inhibition of programmed cell death 4 (PDCD4) [126]. These results suggest that quercetin can regulate the miRNA-21-PDCD4 axis to inhibit malignant transformation of human bronchial epithelial cells induced by Cr(VI)
Summary
Cancer is a chronic consumptive disease that has not been overcome yet and has become a global health problem threatening human life [1, 2]. This study suggests that quercetin and B, in combination, can regulate abnormal epigenetic changes through the HDAC1-IR-NF-kB signaling axis and inhibit growth of the human esophageal cancer cell line Eca9706. Zuo et al found that luteolin can inhibit DNMTs and HDACs in HCT116 and HT29 colon cancer cells and promote Nrf demethylation and upregulate its expression, which activates the Nrf2/antioxidant responsive element(ARE) pathway and inhibits cancer cell proliferation [151] Their results show that luteolin positively regulates the epigenetic effects of anticancer signaling pathways. A study on the effects of luteolin on prostate cancer cells showed that it changed the acetylation state of the gene promoter histone, downregulated expression of 22 key genes of the cell cycle pathway such as cyclin A2 and cyclin E2, and upregulated expression of cyclin-dependent kinase inhibitor 1B [152]. This study suggests that miR-24-1-5p may act as a regulator of the Wnt/bcatenin signaling pathway to inhibit colorectal cancer, which is one of the possible mechanisms of anthocyanin anticancer effects through epigenetic pathways
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
