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  Cell-type-specific role of CHK2 in mediating DNA damage-induced G2 cell cycle arrest

van Jaarsveld, M. T. M., Deng, D., Ordoñez-Rueda, D., Paulsen, M., Wiemer, E. A. C., & Zi, Z. (2020). Cell-type-specific role of CHK2 in mediating DNA damage-induced G2 cell cycle arrest. Oncogenesis, 9: 35. doi:10.1038/s41389-020-0219-y.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0005-EDF0-1 Version Permalink: http://hdl.handle.net/21.11116/0000-0005-EDF1-0
Genre: Journal Article

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van Jaarsveld, Marijn T. M.1, Author              
Deng, Difan1, Author              
Ordoñez-Rueda, Diana , Author
Paulsen, Malte, Author
Wiemer, Erik A. C. , Author
Zi, Zhike1, Author              
Affiliations:
1Cell Signaling Dynamics (Zhike Zi), Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_2117284              

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 Abstract: Cancer is a life-threatening disease that affects one in three people. Although most cases are sporadic, cancer risk can be increased by genetic factors. It remains unknown why certain genes predispose for specific forms of cancer only, such as checkpoint protein 2 (CHK2), in which gene mutations convey up to twofold higher risk for breast cancer but do not increase lung cancer risk. We have investigated the role of CHK2 and the related kinase checkpoint protein 1 (CHK1) in cell cycle regulation in primary breast and lung primary epithelial cells. At the molecular level, CHK1 activity was higher in lung cells, whereas CHK2 was more active in breast cells. Inhibition of CHK1 profoundly disrupted the cell cycle profile in both lung and breast cells, whereas breast cells were more sensitive toward inhibition of CHK2. Finally, we provide evidence that breast cells require CHK2 to induce a G2–M cell cycle arrest in response of DNA damage, whereas lung cells can partially compensate for the loss of CHK2. Our results provide an explanation as to why CHK2 germline mutations predispose for breast cancer but not for lung cancer.

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Language(s): eng - English
 Dates: 2020-02-272020-03-13
 Publication Status: Published online
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 Rev. Method: -
 Identifiers: DOI: 10.1038/s41389-020-0219-y
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Title: Oncogenesis
Source Genre: Journal
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Publ. Info: Nature Publishing Group
Pages: - Volume / Issue: 9 Sequence Number: 35 Start / End Page: - Identifier: ISSN: 2157-9024