Gene expression profile in ulcerative colitis patients: FOXO4, ALDOB, SLC26A3, SOD2 genes as potential biomarkers.

BACKGROUND

Ulcerative colitis (UC) is a complex, chronic inflammatory disease that primarily impacts the colon mucosa. One of the key pathological contributors to the development and progression of inflammatory bowel disease (IBD) is oxidative stress, which results in reactive oxygen species (ROS)-induced mucosal damage. This stress leads to dysfunction of the intestinal barrier.

OBJECTIVES

The purpose of this study is to examine the expression levels of genes involved in various inflammatory pathways, including autophagy, unfolded protein response (UPR), ubiquitination, metabolic pathways, and immune responses in the colon mucosa of patients with UC.

MATERIAL AND METHODS

Patients diagnosed with UC at Çukurova University, Balcalı Hospital, Gastroenterology Department between December 2023 and January 2024 were included in this prospective study. A total of 40 participants were included in the study: 27 ulcerative colitis patients and 13 controls. To isolate high-quality RNA, colon biopsy material obtained during colonoscopy was immediately placed in stabilization solution and stored at - 80 degrees Celsius. The relative quantification of target gene mRNA was determined using a Light Cycler. Subsequently, differences in gene expression between patients and the control group were evaluated using the Mann-Whitney U and Kruskal-Wallis tests.

RESULTS

In our study, FOXO4 gene expression increased in UC patients during both active and remission phases compared to the control group. The high expression of this gene is associated with its role in inflammation and cell death processes. Additionally, the high expression of ALDOB and SLC26A genes is linked to increased inflammation and energy demand. Lastly, the elevated expression of the SOD2 gene can be considered a response to oxidative stress-related inflammatory processes in the disease.

CONCLUSION

These findings propose that these genes could serve as potential biomarkers for genomic identification and understanding the pathogenesis of UC.