Ghrelin promotes oral tumor cell proliferation by modifying GLUT1 expression

作者: Dominik Kraus , Jan Reckenbeil , Matthias Wenghoefer , Helmut Stark , Matthias Frentzen

DOI: 10.1007/S00018-015-2048-2

关键词:

摘要: In our study, ghrelin was investigated with respect to its capacity on proliferative effects and molecular correlations oral tumor cells. The presence of all components the system, i.e., receptors, analyzed could be detected using real-time PCR immunohistochemistry. To examine cellular caused by clarify downstream-regulatory mechanisms, two different cell lines (BHY HN) were used in culture experiments. Stimulation either line led a significantly increased proliferation. Signal transduction occurred through phosphorylation GSK-3β nuclear translocation β-catenin. This effect inhibited blocking protein kinase A. Glucose transporter1 (GLUT1), as an important factor for delivering sufficient amounts glucose cells having high requirements this carbohydrate (Warburg effect) up-regulated exogenous endogenous ghrelin. Silencing intracellular concentrations siRNA significant decreased expression GLUT1 conclusion, study describes role appetite-stimulating peptide hormone cancer proliferation under particular aspect uptake: (1) are source (2) Ghrelin affects autocrine and/or paracrine activity. (3) modulates thus indirectly enhances These findings major relevance, because uptake is assumed promising target treatment.

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