Title of presented paper: The altered expression of GDF11 -- TGF-β family member - during intestinal inflammation and colitis-associated colorectal cancer.

Introduction and aim. Growth differentiation factor 11 (GDF11) is a novel member of TGF-β superfamily. Its role is confirmed in embryogenesis, rejuvenation, and aging. GDF11 is involved in inflammatory response as it inhibits the release of pro-inflammatory cytokines and NLRP3 inflammasome activation. Moreover, GDF11 has clinicopathological signifi- cance in colorectal cancer and is proposed as a possible prognostic factor. The aim of our study is to assess the activity of GDF11 during development of colitis and colorectal cancer in mice. Material and methods. Male C57BL/6 mice were used in our experiments. Colitis was induced by dextran sodium sulfate (DSS) addition into drinking water. Single injection of azoxymethane (AOM) and repeated cycles of DSS were used to induce colitis-associated colorectal cancer. At different time points mice were sacrificed. Human and mouse colorectal cancer cell lines were used in our project to verify GDF11 expression. MC-38 cells were stimulated with the cytokines for 24 hours. We isolated RNA and protein to perform real-time RT-PCR and Western Blot. Statistical analysis was performed using GraphPad Software. Results. We found that GDF11 expression at mRNA level is increased in the mouse colon during aging. GDF11 expression is elevated during the experimental colitis and during the period of recovery. GDF11 expression is changed at initial stage of colorectal cancer in mice. Its expression also differs among different human cell lines. LPS induced an increase of GDF11 expression. Conclusion. We confirmed that GDF11 is crucial at all stages of development of experimental colitis and colitis-associated colorectal cancer. [ABSTRACT FROM AUTHOR]