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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.
Renal cell carcinoma (RCC) is a metabolically active malignancy characterized by dysregulated glucose utilization and mitochondrial dysfunction, suggesting that targeting metabolism could provide therapeutic benefits. Sodium–glucose cotransporter 2 (SGLT2) inhibitors, originally antidiabetic agents, have shown emerging anticancer potential by modulating oncogenic signaling and energy metabolism. However, the metabolic mechanisms underlying SGLT2 inhibition in renal cancer remain unclear. Given that metabolic dependencies in RCC vary with von Hippel–Lindau (VHL) mutation status, investigating SGLT2 inhibitor–induced alterations in VHL–wildtype cells may reveal context-specific vulnerabilities and therapeutic opportunities.
High-resolution LC/MS–based metabolomics was applied to the VHL WT renal cancer cell line Caki1, a model characterized by high metabolic activity and nutrient dependence, to evaluate the metabolic impact of SGLT2 inhibition. Multivariate statistical analyses (PCA, PLS-DA, OPLS-DA) were conducted to identify significantly altered metabolites, which were further subjected to pathway enrichment and network to delineate global metabolic rewiring. Functional validation of pathway-specific alterations was performed through western blotting of key metabolic enzymes.
SGLT2 inhibition induced biphasic metabolic remodeling. Early responses involved activation of fatty acid oxidation (FAO) and the urea cycle, with elevated acetyl-CoA, acylcarnitines, and ketone bodies, accompanied by transient AMPK and PGC-1α activation. Later phases showed sustained upregulation of tricarboxylic acid (TCA) cycle intermediates, nucleotide biosynthesis, and one-carbon metabolism, indicating enhanced mitochondrial function and redox balance restoration. In contrast, lipid and glycine–serine metabolism declined, suggesting reduced mTOR activity and impaired membrane turnover.
SGLT2 inhibition orchestrates coordinated metabolic and signaling reprogramming in VHL–wildtype RCC, shifting energy metabolism toward oxidative balance and growth suppression. These findings provide mechanistic insights into the anticancer potential of SGLT2 inhibitors and support their repositioning as metabolic–signaling modulators for targeted therapy in renal cancer.
