TAILIEUCHUNG - Báo cáo khoa học: Tumor suppressor p16INK4a: Downregulation of galectin-3, an endogenous competitor of the pro-anoikis effector galectin-1, in a pancreatic carcinoma model

The tumor suppressor p16 INK4a has functions beyond cell-cycle control via cyclin-dependent kinases. A coordinated remodeling ofN- and O-glycosyla-tion, and an increase in the presentation of the endogenous lectin galectin-1 sensing these changes on the surface of p16 INK4a -expressing pancreatic carcinoma cells (Capan-1), lead to potent pro-anoikis signals. | Tumor suppressor p16INK4a Downregulation of galectin-3 an endogenous competitor of the pro-anoikis effector galectin-1 in a pancreatic carcinoma model Hugo Sanchez-Ruderisch1 Christian Fischer1 Katharina M. Detjen1 Martina Welzel1 Anja Wimmel1 Joachim C. Manning2 Sabine Andre2 and Hans-Joachim Gabius2 1 Medizinische Klinik . Hepatologie und Gastroenterologie Charite-Universitatsmedizin Berlin Germany 2 Institut fiur Physiologische Chemie Ludwig-Maximilians-Universitat Munchen Germany Keywords anoikis galectin glycosylation integrin pancreatic carcinoma Correspondence K. M. Detjen Charite-Universitatsmedizin Berlin Campus Virchow-Klinikum Med. Klinik . Hepatologie und Gastroenterologie Augustenburger Platz 1 D-13353 Berlin Germany Fax 49 30 450 559939 Tel 49 30 450 559679 E-mail Present address Center for Cardiovascular Research Charite-Universitatsmedizin Berlin Germany Received 20 May 2010 revised 1 July 2010 accepted 5 July 2010 doi The tumor suppressor p16INK4a has functions beyond cell-cycle control via cyclin-dependent kinases. A coordinated remodeling of N- and O-glycosyla-tion and an increase in the presentation of the endogenous lectin galectin-1 sensing these changes on the surface of p16INK4a-expressing pancreatic carcinoma cells Capan-1 lead to potent pro-anoikis signals. We show that the p16INK4a-dependent impact on growth-regulatory lectins is not limited to galectin-1 but also concerns galectin-3. By monitoring its expression in relation to p16INK4a status as well as running anoikis assays with galec-tin-3 and cell transfectants with up- or downregulated lectin expression a negative correlation between anoikis and the presence of this lectin was established. Nuclear run-off and northern blotting experiments revealed an effect of the presence of p16INK4a on steady-state levels of galectin-3-spe-cific mRNA that differed from decreasing the transcriptional rate. On the cell surface .

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• The tumor suppressor p16 INK4a has functions beyond cell cycle control via cyclin dependent kinases
• A coordinated remodeling ofN and O glycosyla tion
• and an increase in the presentation of the endogenous lectin galectin 1 sensing these changes on the surface of p16 INK4a expressing pancreatic carcinoma cells (Capan 1)
• lead to potent pro anoikis signals
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