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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Chronic kidney disease (CKD) is characterized by the accumulation of uremic toxins, including gut dysbiosis-related indoxyl sulfate (IS) and p-cresyl sulfate (p-CS), which are known for their pro-tumorigenic activity. Clinical studies have reported an increased incidence and poorer prognosis of colorectal cancer (CRC) in CKD patients, although the molecular mechanisms underlying this association remain largely unclear. Given their ability to promote tumor aggressiveness, we hypothesized that IS and p-CS contribute to CRC progression under uremic conditions.
Three CRC cell lines (HT-29, HCT 116, and LoVo) were exposed to eight increasing concentrations of IS and p-CS, corresponding to plasma levels observed in CKD patients. Cell proliferation was assessed using the WST-8 assay, while tumorigenic, migratory, and invasive properties were evaluated by clonogenic, wound healing, and invasion assays, respectively. Expression of the inflammatory markers INOS and IL-6 was quantified by Real-Time PCR. Treated cells were subjected to RNA sequencing and bioinformatic analysis to identify differentially expressed genes and modulated pathways, with a focus on the WNT cascade. Since WNT pathway deregulation was specifically observed after IS exposure, validation Real-Time PCR was performed on selected genes (PROM1, LRP5, DKK1, AXIN2). Immunofluorescence was carried out to assess β-catenin subcellular localization, and oxidative stress was evaluated by measuring intracellular reactive oxygen species (ROS) levels.
Exposure to IS and p-CS significantly enhanced proliferation, migration, and invasion in all CRC cell lines. Real-Time PCR analysis showed strong upregulation of INOS and IL-6, indicating activation of inflammatory responses. RNA sequencing revealed that IS, but not p-CS, induced substantial deregulation of the WNT pathway (involved in cell growth and proliferation), with upregulation of PROM1, LRP1, LRP5, and MMP7 and downregulation of DKK1 and AXIN2. These findings were confirmed by validation Real-Time PCR. Immunofluorescence demonstrated WNT-related β-catenin accumulation in both the cytoplasm and nucleus of IS-treated cells, supporting aberrant WNT activation at the protein level. Both toxins also significantly increased intracellular ROS production, confirming oxidative stress induction.
Our findings demonstrate that IS and p-CS promote a more aggressive CRC phenotype under uremic conditions. Specifically, IS drives tumor progression through WNT pathway activation and oxidative stress induction, whereas p-CS appears to act mainly through inflammatory signaling and ROS generation. These results highlight the role of uremic toxins in CRC progression in CKD patients and emphasize the need for further investigation to identify potential therapeutic targets.
