| Online-Ressource |
Verfasst von: | Ryl, Tatsiana [VerfasserIn]  |
| Kuchen, Erika [VerfasserIn]  |
| Shao, Chunxuan [VerfasserIn]  |
| Flórez, Andrés [VerfasserIn]  |
| Mönke, Gregor [VerfasserIn]  |
| Lamprecht, Florian [VerfasserIn]  |
| Höfer, Thomas [VerfasserIn]  |
Titel: | Cell-cycle position of single MYC-driven cancer cells dictates their susceptibility to a chemotherapeutic drug |
Verf.angabe: | Tatsiana Ryl, Erika E. Kuchen, Emma Bell, Chunxuan Shao, Andrés F. Flórez, Gregor Mönke, Sina Gogolin, Mona Friedrich, Florian Lamprecht, Frank Westermann, Thomas Höfer |
E-Jahr: | 2017 |
Jahr: | 23 August 2017 |
Umfang: | 22 S. |
Fussnoten: | Gesehen am 28.05.2018 ; Available online 23 August 2017 |
Titel Quelle: | Enthalten in: Cell systems |
Ort Quelle: | Maryland Heights, MO : Elsevier, 2015 |
Jahr Quelle: | 2017 |
Band/Heft Quelle: | 5(2017,3) Seite 237-250, e1-e8, 22 Seiten |
ISSN Quelle: | 2405-4720 |
Abstract: | Summary: While many tumors initially respond to chemotherapy, regrowth of surviving cells compromises treatment efficacy in the long term. The cell-biological basis of this regrowth is not understood. Here, we characterize the response of individual, patient-derived neuroblastoma cells driven by the prominent oncogene MYC to the first-line chemotherapy, doxorubicin. Combining live-cell imaging, cell-cycle-resolved transcriptomics, and mathematical modeling, we demonstrate that a cell's treatment response is dictated by its expression level of MYC and its cell-cycle position prior to treatment. All low-MYC cells enter therapy-induced senescence. High-MYC cells, by contrast, disable their cell-cycle checkpoints, forcing renewed proliferation despite treatment-induced DNA damage. After treatment, the viability of high-MYC cells depends on their cell-cycle position during treatment: newborn cells promptly halt in G1 phase, repair DNA damage, and form re-growing clones; all other cells show protracted DNA repair and ultimately die. These findings demonstrate that fast-proliferating tumor cells may resist cytotoxic treatment non-genetically, by arresting within a favorable window of the cell cycle. |
DOI: | doi:10.1016/j.cels.2017.07.005 |
URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext ; Verlag: http://dx.doi.org/10.1016/j.cels.2017.07.005 |
| Volltext: http://www.sciencedirect.com/science/article/pii/S2405471217303319 |
| DOI: https://doi.org/10.1016/j.cels.2017.07.005 |
Datenträger: | Online-Ressource |
Sprache: | eng |
Sach-SW: | bistability |
| cancer |
| cell-cycle checkpoints |
| cell-cycle-resolved transcriptomics |
| live-cell imaging |
| mathematical modeling |
| MYC |
| therapy resistance |
K10plus-PPN: | 1575562553 |
Verknüpfungen: | → Zeitschrift |
Cell-cycle position of single MYC-driven cancer cells dictates their susceptibility to a chemotherapeutic drug / Ryl, Tatsiana [VerfasserIn]; 23 August 2017 (Online-Ressource)