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Wnt/β-Catenin Signaling Regulates Telomerase in Stem Cells and Cancer Cells

MPG-Autoren
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Hoffmeyer,  Katrin
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Angelo,  Raggioli
Max Planck Society;

Rudloff,  Stefan
Max Planck Society;

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Hierholzer,  Andreas
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Del Valle,  Ignacio
Department of Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Hein,  Kerstin
Max Planck Society;

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Vogt,  Riana
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Kemler,  Rolf
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Zitation

Hoffmeyer, K., Angelo, R., Rudloff, S., Anton, R., Hierholzer, A., Del Valle, I., et al. (2012). Wnt/β-Catenin Signaling Regulates Telomerase in Stem Cells and Cancer Cells. Science, 336, 1549-1554.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002B-8CF5-D
Zusammenfassung
Telomerase activity controls telomere length and plays a pivotal role in stem cells, aging, and cancer. Here, we report a molecular link between Wnt/β-catenin signaling and the expression of the telomerase subunit Tert. β-Catenin-deficient mouse embryonic stem (ES) cells have short telomeres; conversely, ES cell expressing an activated form of β-catenin (β-catΔEx3/+) have long telomeres. We show that β-catenin regulates Tert expression through the interaction with Klf4, a core component of the pluripotency transcriptional network. β-Catenin binds to the Tert promoter in a mouse intestinal tumor model and in human carcinoma cells. We uncover a previously unknown link between the stem cell and oncogenic potential whereby β-catenin regulates Tert expression, and thereby telomere length, which could be critical in human regenerative therapy and cancer.