Cell cycle control in cancer
Abstract
Cancer is a group of diseases in which cells divide continuously and excessively. Cell division is tightly regulated by multiple evolutionarily conserved cell cycle control mechanisms, to ensure the production of two genetically identical cells. Cell cycle checkpoints operate as DNA surveillance mechanisms that prevent the accumulation and propagation of genetic errors during cell division. Checkpoints can delay cell cycle progression or, in response to irreparable DNA damage, induce cell cycle exit or cell death. Cancer-associated mutations that perturb cell cycle control allow continuous cell division chiefly by compromising the ability of cells to exit the cell cycle. Continuous rounds of division, however, create increased reliance on other cell cycle control mechanisms to prevent catastrophic levels of damage and maintain cell viability. New detailed insights into cell cycle control mechanisms and their role in cancer reveal how these dependencies can be best exploited in cancer treatment.
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CHEK2 is the major downstream target of the cell cycle arrest kinases ATM and ATR.
“Besides the stabilization of PARP1 as a drug target, different proteins stabilized potentially upon phosphorylation, for example, CHEK2, the major downstream target of the cell cycle arrest kinases, ATM, and ATR (Matthews et al, 2022).”
From Network integration of thermal proteome profiling with multi-omics data decodes PARP inhibition (2024) · cites this paper as Matthews et al, 2022
Inclusion of TPP allows retrieval of detailed mechanistic insight into well-known consequences of PARP inhibition, such as DNA damage signaling via the ATM-ATR-CHEK2 axis or cell cycle arrest via modulation of cyclin degradation or the formation of the ESPL1-PTTG1 complex.
“In particular, the inclusion of TPP allows us to retrieve detailed mechanistic insight into well-known consequences of PARP inhibition, such as DNA damage signaling via the ATM-ATR-CHEK2 axis or cell cycle arrest via modulation of cyclin degradation or the formation of the ESPL1-PTTG1 complex (Matthews et al, 2022; Waizenegger et al, 2002).”
From Network integration of thermal proteome profiling with multi-omics data decodes PARP inhibition (2024) · cites this paper as Matthews et al, 2022
Cites
Hallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590 · see citing works
Intratumor Heterogeneity and Branched Evolution Revealed by Multiregion Sequencing
Gerlinger, M., Rowan, A. J., Horswell, S., Larkin, J., Endesfelder, D., Gronroos, E., Martinez, P., Matthews, N., Stewart, A., Tarpey, P., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1113205 · Cited by 7,774 · see citing works
Cell cycle, CDKs and cancer: a changing paradigm
Malumbres, M., & Barbacid, M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2602 · Cited by 3,957 · see citing works
Oncogenic Signaling Pathways in The Cancer Genome Atlas
Sanchez-Vega, F., Mina, M., Armenia, J., Chatila, W. K., Luna, A., La, K. C., Dimitriadoy, S., Liu, D. L., Kantheti, H. S., Saghafinia, S., et al. (2018) · Cell · doi:10.1016/j.cell.2018.03.035 · Cited by 3,201 · see citing works
Causes and consequences of replication stress
Zeman, M. K., & Cimprich, K. A. (2014) · Nature Cell Biology · doi:10.1038/ncb2897 · Cited by 2,079 · see citing works
Ribociclib as first-line therapy for HR-positive, advanced breast cancer
Hortobagyi, G. N., Stemmer, S. M., Burris, H. A., Yap, Y.-S., Sonke, G. S., Paluch-Shimon, S., Campone, M., Blackwell, K. L., André, F., Winer, E. P., et al. (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1609709 · Cited by 2,039 · see citing works
Fry, D. W., Harvey, P. J., Keller, P. R., Elliott, W. L., Meade, M., Trachet, E., Albassam, M., Zheng, X., Leopold, W. R., Pryer, N. K., et al. (2004) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.1427.3.11 · Cited by 1,236 · see citing works
The Cell–Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression
Chen, J. (2016) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a026104 · Cited by 1,222 · see citing works
The multiple mechanisms that regulate p53 activity and cell fate
Hafner, A., Bulyk, M. L., Jambhekar, A., & Lahav, G. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0110-x · Cited by 1,129 · see citing works
Shieh, S.-Y., Ahn, J., Tamai, K., Taya, Y., & Prives, C. (2000) · Genes & Development · doi:10.1101/gad.14.3.289 · Cited by 972 · see citing works
Chk2/hCds1 functions as a DNA damage checkpoint in G<sub>1</sub>by stabilizing p53
Chehab, N. H., Malikzay, A., Appel, M., & Halazonetis, T. D. (2000) · Genes & Development · doi:10.1101/gad.14.3.278 · Cited by 805 · see citing works
Inducing and exploiting vulnerabilities for the treatment of liver cancer
Wang, C., Vegna, S., Jin, H., Benedict, B., Lieftink, C., Ramirez, C., de Oliveira, R. L., Morris, B., Gadiot, J., Wang, W., et al. (2019) · Nature · doi:10.1038/s41586-019-1607-3 · Cited by 427 · see citing works
Barr, A. R., Cooper, S., Heldt, F. S., Butera, F., Stoy, H., Mansfeld, J., Novák, B., & Bakal, C. (2017) · Nature Communications · doi:10.1038/ncomms14728 · Cited by 403 · see citing works
Inhibitors of cyclin-dependent kinases as cancer therapeutics.
Whittaker, S. R., Mallinger, A., Workman, P., & Clarke, P. A. (2017) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.02.008 · Cited by 384 · see citing works
Shamloo, B., & Usluer, S. (2019) · Cancers · doi:10.3390/cancers11081178 · Cited by 336 · see citing works
Senescence as a therapeutically relevant response to CDK4/6 inhibitors
Wagner, V., & Gil, J. (2020) · Oncogene · doi:10.1038/s41388-020-1354-9 · Cited by 148 · see citing works
Rowald, K., Mantovan, M., Passos, J., Buccitelli, C., Mardin, B. R., Korbel, J. O., Jechlinger, M., & Sotillo, R. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.05.048 · Cited by 84 · see citing works
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Protein neddylation and its role in health and diseases
Zhang, S., Yu, Q., Li, Z., Zhao, Y., & Sun, Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01800-9 · Cited by 171 · see citing works
Sun, H., Cai, H., Xu, C., Zhai, H., Lux, F., Xie, Y., Feng, L., Du, L., Liu, Y., Sun, X., et al. (2022) · Journal of Nanobiotechnology · doi:10.1186/s12951-022-01654-9 · Cited by 86 · see citing works
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Burtscher, M. L., Gade, S., Garrido-Rodriguez, M., Rutkowska, A., Werner, T., Eberl, H. C., Petretich, M., Knopf, N., Zirngibl, K., Grandi, P., et al. (2024) · Molecular Systems Biology · doi:10.1038/s44320-024-00025-w · Cited by 7 · see citing works
O-GlcNAcylation of FOXK1 orchestrates the E2F pathway and promotes oncogenesis
Masclef, L., Ahmed, O., Iannantuono, N., Gagnon, J., Gushul-Leclaire, M., Boulay, K., Estavoyer, B., Echbicheb, M., Poy, M., Ali Boubacar, K., et al. (2024) · doi:10.1101/2024.03.01.582838 · Cited by 6 · see citing works
Computational challenges of cell cycle analysis using single cell transcriptomics
Chervov, A., & Zinovyev, A. (2022) · arXiv · doi:10.48550/arxiv.2208.05229 · Cited by 4 · see citing works
- Authors
- Matthews, H. K., Bertoli, C., & de Bruin, R. A. M.
- Affiliations
- MRC Laboratory for Molecular Cell Biology (GB)
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2021-09-10
- Volume
- 23
- Issue
- 1
- Pages
- 74-88
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W3198894769
- Cited by
- 1,506
- References
- 17
- Citations by year
- 2026: 227 · 2025: 398 · 2024: 386 · 2023: 325 · 2022: 156 · 2021: 10 · 2013: 1
- FWCI
- 26.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Cancer Research UK (C1529/A23335, 20147)
- Medical Research Council (MR/K015826/1, MC_EX_G0800785)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- cell cycle regulation, cancer, cell cycle checkpoints, DNA damage response, cell cycle exit, cell death, cancer-associated mutations, cell division, cancer therapy
- MeSH terms
- Animals, DNA Damage, DNA Replication, Humans, Spindle Apparatus, Neoplasms, Oncogenes, Cell Cycle Checkpoints
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