A brand new examine reveals how dietary folate enhances colon most cancers threat in an animal mannequin, emphasizing the want for cautious folate food fortification. This analysis uncovers a direct link between weight-reduction plan and colon most cancers via epigenetic mechanisms, particularly DNA methylation. The findings are vital in understanding environmental influences on most cancers threat and open new avenues for colon most cancers remedy and prevention.
The debate about the function of environmental elements in rising most cancers threat stays unresolved. While epidemiological analysis signifies that parts like weight-reduction plan can contribute to most cancers, significantly in the case of colon most cancers, the actual mechanisms by which dietary elements may enhance most cancers susceptibility are nonetheless unclear.
In a examine printed in Cancer Research Communications, a journal of the American Association for Cancer Research, a workforce led by researchers at Baylor College of Medicine reveals a mechanism by which dietary folate enhances colon most cancers threat in an animal mannequin. The findings additionally spotlight the want for monitoring the long-term security of folate food fortification and ensuing cancer-promoting results, significantly given the rising incidence of early-onset colon most cancers in the United States over the previous 20 years.
Mechanistic Pathway from Diet to Colon Cancer
“In this study we show a mechanistic pathway from diet to colon cancer in an animal model,” mentioned corresponding writer Dr. Lanlan Shen, professor of pediatrics – nutrition at Baylor and a member of the Dan L Duncan Comprehensive Cancer Center. “We investigated whether or not this pathway concerned epigenetics, a system of bookmarking DNA that determines which genes will or won’t be expressed in a cell. Epigenetics is one-way cells can management the actions of their genes with out altering the DNA sequence and is intently linked to the setting.”
Cells bookmark genes by including small chemical modifications to the DNA. Methyl teams are considered one of these chemical modifications, and folate and different related vitamins are instantly concerned in the metabolic pathway resulting in DNA methylation. “Understanding this link between our meals and how our genes work is a big deal. It’s like finding a missing piece of a puzzle we’re getting closer to solving about how to keep our bodies healthy,” Shen mentioned.
Dietary Folate’s Effects on Colon Cancer Development
In the present examine, the researchers examined the impact of dietary folate on colon most cancers improvement of their animal mannequin. The workforce discovered that animals on the folate-supplemented weight-reduction plan had a considerably shortened general survival and extra tumors in addition to bigger tumors in comparison with the animals in the non-supplemented weight-reduction plan. A more in-depth take a look at the tumors revealed the presence of tumor-associated macrophages, a sort of immune cell infiltration that’s clinically related to immunosuppression and poor prognosis in colorectal most cancers sufferers. The tumors additionally had been extremely proliferative.
“Importantly, we observed substantially increased epigenetic methylation of gene p16 – a gene involved in colon cancer development – in animals on the supplemented diet compared to controls,” Shen mentioned. “These findings illuminate a direct link between dietary folate and accelerated tumor development in the colon.”
This examine gives priceless insights into how the setting can affect most cancers threat, opening new avenues to deal with or stop colon most cancers, considered one of the most typical cancers and the second main reason for most cancers loss of life in the United States.
Reference: “Dietary Folate and Cofactors Accelerate Age-dependent p16 Epimutation to Promote Intestinal Tumorigenesis” by Li Yang, Robert C. Peery, Leah M. Farmer, Xia Gao, Yiqun Zhang, Chad J. Creighton, Lanjing Zhang and Lanlan Shen, 19 January 2024, Cancer Research Communications.
DOI: 10.1158/2767-9764.CRC-23-0356
Li Yang, Robert Peery, Leah Farmer, Xia Gao, Yiqun Zhang, Chad J. Creighton and Lanjing Zhang additionally contributed to this examine. The authors are affiliated with a number of of the following establishments: Baylor College of Medicine, Princeton Medical Center, and Rutgers University.
This work was supported by grants from the U.S. Department of Agriculture (CRIS 3092-51000-060) and the National Institutes of Health (R01HD100914 and R01CA233472). Further help was supplied by NIH/NCI grant R00CA237618, USDA 3092-51000-064-05, and the Cancer Prevention and Research Institute of Texas Scholar in Cancer Prevention and Research Award PR210056.
