التفاصيل البيبلوغرافية
| العنوان: |
Planar compression of extracellular substrates induces S phase arrest via ATM-independent CHK2 activation. |
| المؤلفون: |
Hayakawa, Kimihide1, Hirata, Hiroaki1,2, Samsonov, Mikhail3, Sokabe, Masahiro1 msokabe@med.nagoya-u.ac.jp |
| المصدر: |
Biochemical & Biophysical Research Communications. Dec2018, Vol. 506 Issue 4, p983-989. 7p. |
| مصطلحات موضوعية: |
*SERINE/THREONINE kinases, *ENZYME activation, *CELL proliferation, *CELL cycle, *DNA damage, *CHECKPOINT kinase 2 |
| مستخلص: |
Abstract Cell proliferation is regulated not only by soluble chemical factors but also by mechanical cues surrounding cells. Mechanical stretch of extracellular substrates is known to promote cell proliferation by driving exit from the G 0 phase and entry into the S phase. Here, we report that planer compression of extracellular substrates induces cell cycle arrest in the S phase. The compression-induced S phase arrest is mediated by the checkpoint kinase 2 (CHK2)-p53 pathway. In contrast to the canonical S phase checkpoint pathway activated by DNA damage, CHK2 activation by the substrate compression is independent of ataxia telangiectasia mutated (ATM). We further find that disassembly of the actin cytoskeleton is required for the compression-induced S phase arrest. Notably, cancer cells do not exhibit S phase arrest upon the substrate compression. Our results suggest a novel mechanism for homeostatic control of cell growth under mechanical perturbations. Highlights • Planar compression of the extracellular substrate induces S phase arrest. • Cancer cells do not exhibit compression-induced S phase arrest. • The CHK2-p53 pathway mediates compression-induced S phase arrest. • Compression-induced activation of CHK2 is independent of ATM. • Actin disassembly upon substrate compression is required for S phase arrest. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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