In Vivo Investigation of the Effect of Dietary Acrylamide and Evaluation of its Clinical Relevance in Colon Cancer

Dietary exposure to Acrylamide (AA) has been linked with carcinogenicity in the gastrointestinal (GI) tract. However, epidemiologic data on AA intake in relation to cancer risk are limited and contradicting, while the potential cancer-inducing molecular pathways following AA exposure remain elusive. In this study, we collected mechanistic information regarding the induction of carcinogenesis by dietary AA in the colon, using an established animal model. Male Balb/c mice orally received AA (0.1 mg/kg/day) daily for 4 weeks. RNA was extracted from colon tissue samples, followed by RNA sequencing. Comparative transcriptomic analysis between AA and mock-treated groups revealed a set of differentially expressed genes (DEGs) that were further processed using different databases through the STRING-DB portal, to reveal deregulated protein-protein interaction networks. We found that genes implicated in RNA metabolism, processing and formation of the ribosomal subunits and protein translation and metabolism are upregulated in AA-exposed colon tissue; these genes were also overexpressed in human colon adenocarcinoma samples and were negatively correlated with patient overall survival (OS), based on publicly available datasets. Further investigation of the potential role of these genes during the early stages of colon carcinogenesis may shed light into the underlying mechanisms induced by dietary AA exposure. To investigate the effects in colon gene expression patterns of dietary exposure to acrylamide in vivo using mouse models. Male Balb/c mice (n=5 per group) orally received AA (0.1 mg/kg/day) or PBS daily for 4 weeks. RNA was extracted from colon tissue samples, followed by RNA sequencing.