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Investigating the Mechanisms Underlying the Link Between Diabetes and Cancer
Author(s) -
Minch Benjamin,
Englund Dylan,
Sterken Crystal,
LaBounty Zachary,
Kim Jinsil
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.09410
Subject(s) - diabetes mellitus , oxidative stress , cancer , reactive oxygen species , apoptosis , biology , cancer cell , colorectal cancer , medicine , cancer research , endocrinology , microbiology and biotechnology , biochemistry
Diabetes is one of the most common diseases, with its prevalence having increased significantly over the last two decades. A growing number of evidence indicates a higher risk of cancer among patients with diabetes, but the mechanisms underlying the link between diabetes and cancer remain elusive. Hyperglycemia (high blood glucose levels) is a key metabolic abnormality that characterizes diabetes, and could potentially play a role in the pathogenic process of cancer. This study aims to investigate the effects of hyperglycemic conditions on cancer development and progression. The results of cell proliferation assays support cancer‐promoting effects of hyperglycemic conditions in SW620 colorectal cancer cells. High‐glucose treatments, however, did not have any effect on the rate of apoptotic cell death. Analysis of selected RNA‐binding proteins (RBPs) revealed expression changes of the RBPs involved in the methylation of adenosine at the nitrogen‐6 position (N6A) in RNA in response to elevated glucose levels. In line with these changes, there were alterations in N6‐methyladenosine (m 6 A) levels in high glucose‐treated SW620 cells compared to control cells exposed to normal glucose conditions. Our study also suggests that hyperglycemia causes oxidative stress through the production of reactive oxygen species (ROS). Given that elevated levels of ROS and m 6 A RNA methylation have been significantly implicated in human cancer, oxidative stress and altered m 6 A levels caused by dysregulation of the RBPs involved in m 6 A modification may play, at least, a partial role in diabetes‐induced cancer, which warrants future exploration. Collectively, our study provides potentially important insight that could add to the understanding of the mechanisms explaining the link between diabetes and cancer. Support or Funding Information This work was supported by the Stewart Science Honors Program, the School of Science, Technology and Health, and the Department of Biological Sciences at Biola University, CA, USA.