期刊
TRENDS IN CELL BIOLOGY
卷 28, 期 12, 页码 1049-1061出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2018.09.001
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资金
- Deutsche Forschungsgemeinschaft [SFB/TRR 54, SCHM 1633/11-1]
- Helmholtz Association [HA-305]
- Deutsche Krebshilfe [110678]
- Berlin School of Integrative Oncology (BSIO) graduate program
- German Cancer Consortium (GCC)
Activated oncogenes or anticancer therapies evoke senescent cell-cycle arrest in (pre-) malignant cells, thereby interrupting tumor formation or progression. Physiologically, cellular senescence contributes to embryonic development and tissue regeneration. These observations and the overlap of numerous gene products in senescence and stem cell signaling prompted investigations into whether epigenetic establishment of the senescent state may concomitantly reprogram the cell into a latent stem-like condition, whose functional impact becomes evident when arrested cells resume proliferation. We review here recent discoveries underscoring the unexpected senescence-stemness alliance, elucidate underlying molecular mechanisms, and discuss its fundamentally different implications in normal tissue repair - to replenish the exhausted repopulation capacity - as compared to cancer biology, where usurpation of this natural principle accounts for particularly aggressive tumor behavior.
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