Abstract
The SLC25A32 gene plays a pivotal regulatory role in one-carbon metabolism and redox balance by functioning as a transporter for tetrahydrofolate and flavin adenine dinucleotide (FAD). The probable contribution of SLC25A32 toward facilitating the proliferation of cancerous cells remains inadequately explored. This pilot study aims to survey the expression of SLC25A32 in non-metastatic colorectal tissues and its potential association with clinicopathological characteristics. Fresh tissue samples were collected from 30 colorectal cancer patients and their adjacent normal tissues. Total RNA was extracted, and cDNA was synthesized for qRT-PCR. In silico analysis was also performed to further investigate the functional significance of SLC25A32 in colorectal cancer by examining its expression in normal tissues, identifying protein interactions, and searching for pathogenic mutations. Our results revealed a significant up-regulation of SLC25A32 expression in tumorous tissues compared to non-tumorous tissues. The elevated expression of SLC25A32 was associated with tumor anatomic site and size. In silico analysis revealed that higher levels of SLC25A32 expression were correlated with reduced overall survival rates. Furthermore, enrichment analysis showed that this gene remarkably enriched in the process of Folate metabolism. The involvement of SLC25A32 in tumorigenesis may be due to its regulation of mitochondrial folate and FAD metabolism, which have been linked to cancer progression. Changes in SLC25A32 expression or function may contribute to cancer development, making it a potential therapeutic target for cancer treatment.