BACTERIA-INDUCED STEM CELL REPROGRAMMING IN COLON CANCER

Colorectal cancer (CRC) is the third most common malignancy worldwide and remains associated with high mortality. Epidemiological and statistical studies have linked bacterial infections, particularly Salmonella, to an increased risk of CRC development. While this epidemiological association is well documented, as is the glycolytic reprogramming that characterizes tumor cells, it is unclear whether bacteria directly contribute to tumorigenesis via modulating glucose metabolism. I investigated the impact of bacterial infections on glycolytic host cells using organoid models. These three-dimensional culture systems provide a physiologically relevant model to study host–microbe interactions in vitro. Organoids were established from healthy (WT) and predisposed APCMin mouse tissue, the latter harbouring inactivated adenomatous polyposis coli (APC) gene, one of the earliest events in CRC initiation. Organoids were infected with Salmonella, and analyses included immunostaining, qPCR, and FACS to assess changes in gene expression and cellular populations. In addition, I monitored organoid growth and examined the expression of genes involved in glucose metabolism and cell proliferation under different infection conditions. Although no significant differences were detected, likely due to the limited dataset, this study establishes an experimental framework to explore how bacterial pathogens may influence cellular metabolism and contribute to glycolytic reprogramming in colorectal tumorigenesis.