TY - JOUR
T1 - Epigenetic Modifications as Novel Therapeutic Strategies of Cancer Chemoprevention by Phytochemicals
AU - Hsieh, Hui Hsia
AU - Kuo, Min Zhan
AU - Chen, I. An
AU - Lin, Chien Ju
AU - Hsu, Victor
AU - HuangFu, Wei Chun
AU - Wu, Tien Yuan
N1 - Publisher Copyright:
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.
PY - 2025
Y1 - 2025
N2 - Purpose: Epigenetic modifications, such as aberrant DNA methylation, histone alterations, non-coding RNA remodeling, and modulation of transcription factors, are pivotal in the pathogenesis of diverse malignancies. Reactive oxygen species (ROS) have the capacity to impact these epigenetic mechanisms, including DNA methylation, throughout the different stages of cancer development. Therefore, the aim of this review is to address the impact of. Methods: Published papers were searched in Pubmed and Google Scholar databases using the keywords “epigenetic”, or “DNA methylation”, or “phytochemicals”, or “chemoprevention” to prepare this review. Results: There is mounting evidence indicating that diminishing ROS accumulation within cells can regulate the function of DNA methyltransferases (DNMTs). Moreover, activation of the cellular defense system can impede and potentially reverse the progression of tumors in cancerous cells. As a result, ROS scavengers, antioxidants, and demethylating agents have emerged as potential therapeutic approaches for specific types of cancer. Additionally, dietary phytochemicals present in fruits, vegetables, and herbs, which have been utilized for centuries, exhibit the capability to modulate transcription factors, decrease inflammation, deliver antioxidant benefits, induce cell-cycle arrest, and stimulate apoptosis. Conclusion: These phytochemicals can also renew and reprogram the expression of genes that suppress cancer. Thus, prolonged exposure to phytochemicals at low doses represents an innovative therapeutic tactic for the prevention of cancer.
AB - Purpose: Epigenetic modifications, such as aberrant DNA methylation, histone alterations, non-coding RNA remodeling, and modulation of transcription factors, are pivotal in the pathogenesis of diverse malignancies. Reactive oxygen species (ROS) have the capacity to impact these epigenetic mechanisms, including DNA methylation, throughout the different stages of cancer development. Therefore, the aim of this review is to address the impact of. Methods: Published papers were searched in Pubmed and Google Scholar databases using the keywords “epigenetic”, or “DNA methylation”, or “phytochemicals”, or “chemoprevention” to prepare this review. Results: There is mounting evidence indicating that diminishing ROS accumulation within cells can regulate the function of DNA methyltransferases (DNMTs). Moreover, activation of the cellular defense system can impede and potentially reverse the progression of tumors in cancerous cells. As a result, ROS scavengers, antioxidants, and demethylating agents have emerged as potential therapeutic approaches for specific types of cancer. Additionally, dietary phytochemicals present in fruits, vegetables, and herbs, which have been utilized for centuries, exhibit the capability to modulate transcription factors, decrease inflammation, deliver antioxidant benefits, induce cell-cycle arrest, and stimulate apoptosis. Conclusion: These phytochemicals can also renew and reprogram the expression of genes that suppress cancer. Thus, prolonged exposure to phytochemicals at low doses represents an innovative therapeutic tactic for the prevention of cancer.
KW - chemoprevention
KW - DNA methylation
KW - epigenetic
KW - phytochemicals
KW - chemoprevention
KW - DNA methylation
KW - epigenetic
KW - phytochemicals
UR - http://www.scopus.com/inward/record.url?scp=85214646956&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85214646956&partnerID=8YFLogxK
U2 - 10.1007/s11095-024-03810-2
DO - 10.1007/s11095-024-03810-2
M3 - Article
AN - SCOPUS:85214646956
SN - 0724-8741
VL - 42
SP - 69
EP - 78
JO - Pharmaceutical Research
JF - Pharmaceutical Research
IS - 1
M1 - 111502
ER -