Senescence-associated reprogramming promotes cancer stemness
Senescence-associated reprogramming promotes cancer stemness
Nature 553, 7686 (2018). doi:10.1038/nature25167
Authors: Maja Milanovic, Dorothy N. Y. Fan, Dimitri Belenki, J. Henry M. Däbritz, Zhen Zhao, Yong Yu, Jan R. Dörr, Lora Dimitrova, Dido Lenze, Ines A. Monteiro Barbosa, Marco A. Mendoza-Parra, Tamara Kanashova, Marlen Metzner, Katharina Pardon, Maurice Reimann, Andreas Trumpp, Bernd Dörken, Johannes Zuber, Hinrich Gronemeyer, Michael Hummel, Gunnar Dittmar, Soyoung Lee & Clemens A. Schmitt
Cellular senescence is a stress-responsive cell-cycle arrest program that terminates
the further expansion of (pre-)malignant cells. Key signalling
components of the senescence machinery, such as p16INK4a,
p21CIP1 and p53, as well as trimethylation of lysine 9 at histone
H3 (H3K9me3), also operate as critical regulators of stem-cell functions (which are
collectively termed ‘stemness’). In cancer
cells, a gain of stemness may have profound implications for tumour aggressiveness
and clinical outcome. Here we investigated whether chemotherapy-induced senescence
could change stem-cell-related properties of malignant cells. Gene expression and
functional analyses comparing senescent and non-senescent B-cell lymphomas from
Eμ-Myc transgenic mice revealed substantial upregulation of
an adult tissue stem-cell signature, activated Wnt signalling, and distinct
...
Source: Nature - Category: Research Authors: Maja Milanovic Dorothy N. Y. Fan Dimitri Belenki J. Henry M. D äbritz Zhen Zhao Yong Yu Jan R. D örr Lora Dimitrova Dido Lenze Ines A. Monteiro Barbosa Marco A. Mendoza-Parra Tamara Kanashova Marlen Metzner Katharina Pardon Maurice Reimann Andreas Trump Tags: Letter Source Type: research
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