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Cell cycle, CDKs and cancer: a changing paradigm
Abstract
Tumour-associated cell cycle defects are often mediated by alterations in cyclin-dependent kinase (CDK) activity. Misregulated CDKs induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, mammalian CDKs are essential for driving each cell cycle phase, so therapeutic strategies that block CDK activity are unlikely to selectively target tumour cells. However, recent genetic evidence has revealed that, whereas CDK1 is required for the cell cycle, interphase CDKs are only essential for proliferation of specialized cells. Emerging evidence suggests that tumour cells may also require specific interphase CDKs for proliferation. Thus, selective CDK inhibition may provide therapeutic benefit against certain human neoplasias.
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“In contrast, the demonstration that inactivation of these genes can prevent oncogene-induced tumor development in mouse models reinforced the view that these enzymes might be suitable cancer-specific drug targets (65).”
From Targeting CDK4 and CDK6: From Discovery to Therapy (2016) · cites this paper as [65]
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Cites
1 retracted
Fasano, C. A., Dimos, J. T., Ivanova, N. B., Lowry, N. A., Lemischka, I. R., & Temple, S. (2007) · Cell stem cell · doi:10.1016/j.stem.2007.04.001 · Cited by 308
RetractedTargeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
Farmer, H., McCabe, N., Lord, C. J., Tutt, A. N. J., Johnson, D. A., Richardson, T. B., Santarosa, M., Dillon, K. J., Hickson, I., Knights, C., et al. (2005) · Nature · doi:10.1038/nature03445 · Cited by 6,683
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
Lane, D. P. (1992) · Nature · doi:10.1038/358015a0 · Cited by 5,138
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
p21 is a universal inhibitor of cyclin kinases
Xiong, Y., Hannon, G., Zhang, H., Casso, D., Kobayashi, R., & Beach, D. (1993) · Nature · doi:10.1038/366701a0 · Cited by 3,691
A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4.
Serrano, M., Hannon, G. J., & Beach, D. (1993) · Nature · doi:10.1038/366704a0 · Cited by 3,650
Patterns of somatic mutation in human cancer genomes
Greenman, C. D., Stephens, P., Smith, R., Dalgliesh, G. L., Hunter, C., Bignell, G. R., Davies, H. R., Teague, J. W., Butler, A. P., Stevens, C., et al. (2007) · Nature · doi:10.1038/nature05610 · Cited by 3,143
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047
Cell-cycle checkpoints and cancer
Kastan, M. B., & Bartek, J. (2004) · Nature · doi:10.1038/nature03097 · Cited by 2,836
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Research works printed but not linked: 1
- Hanks, S. et al. Constitutional aneuploidy and cancer predisposition caused by biallelic mutations in BUB1B. Nature Genet. 36, 1159–1161 (2004). · DOI
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Sorted by citations
Items 301–400 of 1,005
Metabolic and colonic microbiota transformation may enhance the bioactivities of dietary polyphenols
Chiou, Y., Wu, J.-C., Huang, Q., Shahidi, F., Wang, Y., Ho, C., & Pan, M. (2013) · Journal of Functional Foods · doi:10.1016/j.jff.2013.08.006 · Cited by 113
Wu, X., Song, M., Qiu, P., Li, F., Wang, M., Zheng, J., Wang, Q., Xu, F., & Xiao, H. (2017) · Food & Function · doi:10.1039/c7fo01155e · Cited by 113
CDK12 controls G1/S progression by regulating RNAPII processivity at core DNA replication genes
Manavalan, A. P. C., Pilařová, K., Kluge, M., Bartholomeeusen, K., Rájecký, M., Oppelt, J., Khirsariya, P., Paruch, K., Krejčí, L., Friedel, C. C., et al. (2019) · EMBO Reports · doi:10.15252/embr.201847592 · Cited by 114
“The protein levels of numerous cell cycle regulators fluctuate during cell cycle progression according to their function in a specific phase [38].”
Zhang, D., Liu, J.-S., Tang, M.-K., Yiu, A., Cao, H., Jiang, L., Chan, J. Y., Tian, H., Fung, K., & Ye, W. (2012) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2012.06.045 · Cited by 112
Chemoprevention of Breast Cancer by Dietary Polyphenols
Mocanu, M., Nagy, P., & Szöllõsi, J. (2015) · Molecules · doi:10.3390/molecules201219864 · Cited by 114
Carr, S. M., Munro, S., Kessler, B. M., Oppermann, U. C. T., & Thangue, N. B. L. (2010) · The EMBO Journal · doi:10.1038/emboj.2010.311 · Cited by 115
“pRb is an established and important tumour suppressor (Weinberg, 1995; Dyson, 1998; Stevens and La Thangue, 2003) and a well-characterized target for Cdk activity (Morgan, 1997; Malumbres and Barbacid, 2009).”
BackgroundPerspective of Cyclin-dependent kinase 9 (CDK9) as a Drug Target
Kryštof, V., Baumli, S., & Fürst, R. (2012) · Current Pharmaceutical Design · doi:10.2174/138161212800672750 · Cited by 112
“Besides transcription, CDKs regulate other cellular processes and were originally identified as the core of the cell cycle control system [3,21].”
BackgroundJohnson, N., & Shapiro, G. I. (2010) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.2010.525221 · Cited by 113
“Cdk2 and cdk1, together, direct S and G2 phase transit, while cdk1 governs the G2/M transition and mitotic progression [2-4].”
Targeting the Checkpoint to Kill Cancer Cells
Benada, J., & Macůrek, L. (2015) · Biomolecules · doi:10.3390/biom5031912 · Cited by 115
“Cell proliferation is tightly regulated by cyclin-dependent kinases suggesting their potential use as pharmacological targets in cancer therapy [150,151].”
BackgroundHighlights in Resistance Mechanism Pathways for Combination Therapy
Delou, J. M. D. A., Souza, A. S. O., Souza, L. C. D. M. E., & Borges, H. L. (2019) · Cells · doi:10.3390/cells8091013 · Cited by 118
“There are 13 members of the CDK family, from which only four—CDK1, CDK2, CDK4, and CDK6— are direct regulators of the cell cycle [69].”
Diao, P.-C., Lin, W.-Y., Jian, X., Li, Y., You, W., & Zhao, P. (2019) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2019.06.055 · Cited by 110
Integrated proteogenomic characterization of urothelial carcinoma of the bladder
Xu, N., Yao, Z., Shang, G., Ye, D., Wang, H., Zhang, H., Qu, Y., Xu, F., Wang, Y., Qin, Z., et al. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01291-7 · Cited by 115
“Among these kinases, CDK1 is reportedly the only essential member of the CDK subfamily, which plays an important role in cell cycle progression [59].”
BackgroundProtein conformational ensembles in function: roles and mechanisms
Nussinov, R., Liu, Y., Zhang, W., & Jang, H. (2023) · RSC Chemical Biology · doi:10.1039/d3cb00114h · Cited by 122
p38 MAPK: A dual role in hepatocyte proliferation through reactive oxygen species
Tormos, A. M., Taléns‐Visconti, R., Nebreda, Á. R., & Sastre, J. (2013) · Free Radical Research · doi:10.3109/10715762.2013.821200 · Cited by 112
Palbociclib (PD 0332991): targeting the cell cycle machinery in breast cancer
Rocca, A., Farolfi, A., Bravaccini, S., Schirone, A., & Amadori, D. (2013) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.2014.870555 · Cited by 112
“CDKs are also involved in DNA-damage checkpoints.”
BackgroundInfluentialSmad phosphoisoform signaling specificity: the right place at the right time
Matsuzaki, K. (2011) · Carcinogenesis · doi:10.1093/carcin/bgr172 · Cited by 114
Pabla, N., Gibson, A. A., Buege, M., Ong, S. S., Li, L., Hu, S., Du, G., Sprowl, J. A., Vasilyeva, A., Janke, L. J., et al. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1424313112 · Cited by 110
“C division is a fundamental biological process that is tightly regulated by evolutionarily conserved signaling pathways (1, 2).”
BackgroundInfluentialIntegrating the DNA damage and protein stress responses during cancer development and treatment
Gorgoulis, V. G., Pefani, D., Pateras, I. S., & Trougakos, I. P. (2018) · The Journal of Pathology · doi:10.1002/path.5097 · Cited by 108
“In mammals, several CDK–cyclin complexes are essential for normal proliferation [108].”
BackgroundStockwell, S. R., Platt, G., Barrie, S. E., Zoumpoulidou, G., Poele, R. T., Aherne, G. W., Wilson, S. C., Sheldrake, P. W., McDonald, E., Venet, M., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0028568 · Cited by 107
“However, a considerable level of functional redundancy appears to exist amongst members of this kinase family, and a full complement of G1/S regulatory cyclinCDK complexes may be essential in some but not other cell types [17,18], suggesting that effective checkpoint activation through inhibition of these enzymes coul…”
BackgroundAlajmi, M. F., Rehman, M. T., Hussain, A., & Rather, G. M. (2018) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2018.05.023 · Cited by 110
Molecular crosstalk between cancer and neurodegenerative diseases
Seo, J., & Park, M. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03428-3 · Cited by 109
Prediction of intracellular exposure bridges the gap between target- and cell-based drug discovery
Mateus, A., Gordon, L. J., Wayne, G. J., Almqvist, H., Axelsson, H., Seashore-Ludlow, B. A., Treyer, A., Matsson, P., Lundbäck, T., West, A., et al. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1701848114 · Cited by 106
CDK inhibitors from past to present: A new wave of cancer therapy
Jameel, M., Bhadresha, K. P., & Kwok, H. F. (2022) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2022.12.006 · Cited by 111
Geraniol inhibits prostate cancer growth by targeting cell cycle and apoptosis pathways
Kim, S.-H., Bae, H. C., Park, E., Lee, C. R., Kim, B.-J., Lee, S., Park, H. H., Kim, S. J., So, I., Kim, T., et al. (2011) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2011.02.124 · Cited by 106
A novel long non-coding RNA-ARA: Adriamycin Resistance Associated
Jiang, M., Huang, O., Xie, Z., Wu, S., Zhang, X., Shen, A., Liu, H., Chen, X., Wu, J., Lou, Y., et al. (2013) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.10.020 · Cited by 107
The antitumor activity of the fungicide ciclopirox
Zhou, H., Shen, T., Luo, Y., Liu, L., Chen, W., Xu, B., Han, X., Pang, J., Rivera, C. A., & Huang, S. (2010) · International Journal of Cancer · doi:10.1002/ijc.25255 · Cited by 109
“During distinct phases of the cell cycle, cyclin/CDK complexes are formed and can guide the CDKs to appropriate substrates and activate their catalytic activity.(15) Early G1 transition is mainly regulated by cyclin D complexed with CDK4 and/or CDK6, whereas late G1-S and early S-phase transitions are regulated by cyc…”
BackgroundMethodInfluentialHeathcote, D. A., Patel, H., Kroll, S. H. B., Hazel, P., Periyasamy, M., Alikian, M., Kanneganti, S. K., Jogalekar, A. S., Scheiper, B., Barbazanges, M., et al. (2010) · Journal of Medicinal Chemistry · doi:10.1021/jm100732t · Cited by 105
Cdk2 is required for p53-independent G2/M checkpoint control
Chung, J. H., & Bunz, F. (2010) · PLoS Genetics · doi:10.1371/journal.pgen.1000863 · Cited by 105
Exploiting polypharmacology for drug target deconvolution
Gujral, T. S., Peshkin, L., & Kirschner, M. W. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1403080111 · Cited by 102
Etemadmoghadam, D., George, J., Cowin, P. A., Cullinane, C. M., Kansara, M., Chenevix‐Trench, G., Gorringe, K. L., Smyth, G. K., & Bowtell, D. D. L. (2010) · PLoS ONE · doi:10.1371/journal.pone.0015498 · Cited by 105
“To date, the clinical success of single-agent CDK inhibitors has been disappointing [34].”
BackgroundInhibition of Rb Phosphorylation Leads to mTORC2-Mediated Activation of Akt
Zhang, J., Xu, K. L., Liu, P., Geng, Y., Wang, B., Gan, W., Guo, J., Wu, F., Chin, Y. R., Berrios, C. J., et al. (2016) · Molecular Cell · doi:10.1016/j.molcel.2016.04.023 · Cited by 107
“Given that the CDK4/6-cyclin D-Rb pathway has recently emerged as an attractive drug target for cancer therapies (Malumbres and Barbacid, 2009) and CDK4/6 inhibitors (including PD0332991, LEE011, and LY2835219) have shown promising clinical outcomes (Brower, 2014; Mayer, 2015), we next examined whether pharmacological…”
Prognostic and predictive values of CDK1 and MAD2L1 in lung adenocarcinoma
Shi, Y.-X., Zhu, T., Zou, T., Zhuo, W., Chen, Y., Huang, M., Zheng, W., Wang, C., Li, X., Mao, X., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.13252 · Cited by 105
“Cyclin-dependent kinases (CDKs) are important cell cycle-regulating proteins [16].”
Wang, Y., Liu, J., Yang, J., Yu, X., Chen, Z., Chen, Y., Kuang, M., Zhu, Y., & Zhuang, S. (2019) · Hepatology · doi:10.1002/hep.30613 · Cited by 105
“The deregulation of cell cycle progression, particularly the G1/S transition, is a common feature of cancer cells, and targeting cell cycle pathways has been considered a promising strategy for cancer therapy.(6,26) CDK6 is the key driver of G1/S transition and cell division,(7) and its expression and activity are tig…”
BackgroundTransient Hysteresis in CDK4/6 Activity Underlies Passage of the Restriction Point in G1
Chung, M., Liu, C., Yang, H. W., Köberlin, M. S., Cappell, S. D., & Meyer, T. (2019) · Molecular Cell · doi:10.1016/j.molcel.2019.08.020 · Cited by 117
“Using live-cell tracking of cyclin E/A-CDK activity followed by fixation and single-molecule RNA fluorescence in situ hybridization (FISH) analysis, we found that inhibition of CDK4/6 in cells with high cyclin E/A-CDK activity significantly inhibited expression of the E2F target genes E2F1 and CCNE1 (Figure 3F).”
BackgroundInfluentialMathieu, J., Cauvin, C., Moch, C., Radford, S. J., Sampaio, P., Perdigoto, C. N., Schweisguth, F., Bardin, A. J., Sunkel, C. E., McKim, K. S., et al. (2013) · Developmental Cell · doi:10.1016/j.devcel.2013.07.005 · Cited by 105
“A highCdk-1 activity, mostly driven byCyclin B/Cdk-1 in higher eukaryotes, allows the cell to enter and performmitosis (Malumbres and Barbacid, 2009).”
BackgroundNeganova, I. E., Tilgner, K., Buskin, A., Paraskevopoulou, I., Atkinson, S. P., Peberdy, D., Passos, J. F., & Lako, M. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.464 · Cited by 103
“regulation in human pluripotent stem cells, we focused on a key cell cycle regulator, cyclindependent kinase 1 (Cdk1).(11)”
BackgroundCdk1/Cyclin B1 Controls Fas-Mediated Apoptosis by Regulating Caspase-8 Activity
Matthess, Y., Raab, M., Sanhaji, M., Lavrik, I. N., & Strebhardt, K. (2010) · Molecular and Cellular Biology · doi:10.1128/mcb.00731-10 · Cited by 105
Cell cycle-dependent control of homologous recombination
Zhao, X., Wei, C., Li, J., Xing, P., Li, J., Zheng, S., & Chen, X. (2017) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmx055 · Cited by 113
Ying, M., Shao, X., Jing, H., Liu, Y., Qi, X., Cao, J., Chen, Y., Xiang, S., Song, H., Hu, R., et al. (2018) · Blood · doi:10.1182/blood-2017-10-813139 · Cited by 105
The effect of paclitaxel on apoptosis, autophagy and mitotic catastrophe in AGS cells
Khing, T. M., Choi, W. S., Kim, D., Po, W. W., Thein, W., Shin, C. Y., & Sohn, U. D. (2021) · Scientific Reports · doi:10.1038/s41598-021-02503-9 · Cited by 109
Coupling the cell cycle to development
Budirahardja, Y., & Gönczy, P. (2009) · Development · doi:10.1242/dev.021931 · Cited by 102
“This group of kinases is referred to as cyclin-dependent kinases (Cdks), as kinase activity requires the presence of the cyclin (reviewed by Malumbres and Barbacid, 2009).”
BackgroundA Novel CDK9 Inhibitor Shows Potent Antitumor Efficacy in Preclinical Hematologic Tumor Models
Yin, T., Lallena, M. J., Kreklau, E. L., Fales, K. R., Carballares, S., Torrres, R., Wishart, G. N., Ajamie, R. T., Cronier, D. M., Iversen, P. W., et al. (2014) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-13-0849 · Cited by 104
Bone morphogenetic protein 4—a fascinating regulator of cancer cell behavior
Kallioniemi, A. H. (2012) · Cancer Genetics · doi:10.1016/j.cancergen.2012.05.009 · Cited by 105
Sonntag, R., Giebeler, N., Nevzorova, Y. A., Bangen, J., Fahrenkamp, D., Lambertz, D., Haas, U., Hu, W., Gaßler, N., Cubero, F. J., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1807155115 · Cited by 103
“Specific cyclin/Cdk complexes regulate transition through the distinct phases of the cell cycle by phosphorylation of phasespecific substrates (1).”
BackgroundSelf-citationMultiple effects of CDK4/6 inhibition in cancer: From cell cycle arrest to immunomodulation
Bonelli, M. A., Monica, S. L., Fumarola, C., & Alfieri, R. R. (2019) · Biochemical Pharmacology · doi:10.1016/j.bcp.2019.113676 · Cited by 104
Compression-induced dedifferentiation of adipocytes promotes tumor progression
Li, Y., Mao, A. S., Seo, B. R., Zhao, X., Gupta, S. K., Chen, M., Han, Y., Shih, T., Mooney, D. J., & Guo, M. (2020) · Science Advances · doi:10.1126/sciadv.aax5611 · Cited by 103
Dissecting the Pol II transcription cycle and derailing cancer with CDK inhibitors
Parua, P. K., & Fisher, R. P. (2020) · Nature Chemical Biology · doi:10.1038/s41589-020-0563-4 · Cited by 105
Igal, R. A. (2011) · Cancers · doi:10.3390/cancers3022462 · Cited by 103
“Finally, although the molecular mechanisms by which SCD1 influences cell cycle are largely unknown, recent data indicate that SCD1 may control cell cycle by altering the levels of cyclin D1 and CDK6 [23], two proteins involved in the progression of cycling cells through G1 phase [37].”
BackgroundChen, W., Luo, Y., Liu, L., Zhou, H., Xu, B., Han, X., Shen, T., Liu, Z., Lu, Y., & Huang, S. (2010) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-10-0020 · Cited by 103
“Of the cell cycle–related cyclins, cyclins D and E play an important role in the transition from the G1 to the S phase, and cyclin D1-CDK4/6 and cyclin ECDK2 complexes are required for G1 progression (1).”
BackgroundInfluentialResponse of MicroRNAs to In Vitro Treatment with Graphene Oxide
Li, Y., Wu, Q., Zhao, Y., Bai, Y., Chen, P., Xia, T., & Wang, D. (2014) · ACS Nano · doi:10.1021/nn4065378 · Cited by 102
An update on the implications of cyclin D1 in oral carcinogenesis
Ramos‐García, P., Montoya, J. A. G., Scully, C. M., Ayén, Á., González‐Ruiz, L., Navarro‐Triviño, F. J., & González‐Moles, M. Á. (2016) · Oral Diseases · doi:10.1111/odi.12620 · Cited by 104
Sabbaghi, M., Gil‐Gómez, G., Guardia, C., Servitja, S., Arpí, O., García‐Alonso, S., Menéndez, S., Arumí-Uría, M., Serrano, L., Salido, M., et al. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-17-0696 · Cited by 110
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BackgroundBuzdin, A. A., Sorokin, M., Garazha, A., Sekacheva, M. I., Kim, E. L., Zhukov, N. V., Wang, Y., Li, X., Kar, S., Hartmann, C. J., et al. (2018) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2018.06.003 · Cited by 103
Chohan, T. A., Qayyum, A., Rehman, K., Tariq, M., & Akash, M. S. H. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.08.116 · Cited by 102
Fu, S., Yao, S., Yuan, Y., Previs, R. A., ELIAS, A. D., Carvajal, R. D., George, T. J., Yuan, Y., Yu, L., Westin, S. N., et al. (2022) · Journal of Clinical Oncology · doi:10.1200/jco.22.00830 · Cited by 102
“, median (range) 3 (1-7) Prior radiation therapy, No.”
BackgroundReversal of Resistance towards Cisplatin by Curcumin in Cervical Cancer Cells
Roy, M., & Mukherjee, S. (2014) · Asian Pacific Journal of Cancer Prevention · doi:10.7314/apjcp.2014.15.3.1403 · Cited by 102
“Cyclin D1 and CDK4, member of the cyclin family plays an important role in G1-S transition (Malumbres and Barbacid, 2009) CDKs are known to phosphorylate pRb, releasing E2F from the cytoplasm, therefore effect of curcumin on CDKs was observed.”
BackgroundUitdehaag, J. C. M., Verkaar, F., Alwan, H. A. J., de Man, J., Buijsman, R. C., & Zaman, G. J. R. (2012) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2012.01859.x · Cited by 103
“CDKs are highly pursued potential cancer drug targets (Malumbres and Barbacid, 2009).”
BackgroundXie, R., Chen, X., Chen, Z., Huang, M. X., Dong, W., Gu, P., Zhang, J., Zhou, Q., Dong, W., Han, J., et al. (2019) · Cancer Letters · doi:10.1016/j.canlet.2019.01.041 · Cited by 100
p38γ is essential for cell cycle progression and liver tumorigenesis
Tomás‐Loba, A., Manieri, E., González‐Terán, B., Mora, A., Leiva‐Vega, L., Santamans, A. M., Romero-Becerra, R., Rodríguez, E., Chocano, A. P., Feixas, F., et al. (2019) · Nature · doi:10.1038/s41586-019-1112-8 · Cited by 103
Self-citationOhoka, N., Nagai, K., Hattori, T., Okuhira, K., Shibata, N., Cho, N. J., & Naito, M. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.471 · Cited by 100
Sigma-2 ligands induce tumour cell death by multiple signalling pathways
Zeng, C., Rothfuss, J., Zhang, J., Chu, W., Vangveravong, S., Tu, Z., Pan, F., Chang, K. C., Hotchkiss, R., & Mach, R. H. (2012) · British Journal of Cancer · doi:10.1038/bjc.2011.602 · Cited by 94
“It is well known that D-type cyclins are responsible for progression through G1 phase; E-type cyclins for completion of G1 phase and entry into S-phase; A-type cyclins for driving the transition from S-phase to M-phase (G2 phase); and B-type cyclins for cell progression through M-phase (Malumbres and Barbacid, 2009).”
BackgroundInfluentialWei, D., Parsels, L. A., Karnak, D. M., Davis, M. A., Parsels, J. D., Marsh, A. C., Zhao, L., Maybaum, J., Lawrence, T. S., Sun, Y., et al. (2013) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-13-0788 · Cited by 100
“First, based on the well-established role of CDK1 in mitotic entry, LB100 may promote aberrant entry into mitosis following radiation (39).”
Hu, Y., Kang, C., Zhao, J., Nie, Y., Zheng, L., Li, H., Li, X., Wang, Q., & Qiu, Y. (2017) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13338 · Cited by 100
“CDK2 regulates the G1/S transition [28].”
BackgroundEvidence that the human cell cycle is a series of uncoupled, memoryless phases
Chao, H. X., Fakhreddin, R. I., Shimerov, H. K., Kedziora, K. M., Kumar, R. J., Perez, J., Limas, J. C., Grant, G. D., Cook, J. G., Gupta, G. P., et al. (2019) · Molecular Systems Biology · doi:10.15252/msb.20188604 · Cited by 100
“This observation may be explained by the fewer number of cell cycle regulators in yeast (Malumbres & Barbacid, 2009; Lim & Kaldis, 2013) or a more dominant role for cell size control (Garmendia-Torres et al , 2018), or both.”
Anticancer mechanism of coumarin-based derivatives
Yadav, A. K., Shrestha, R. M., & Yadav, P. N. (2024) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2024.116179 · Cited by 110
Multiple E2F-Induced MicroRNAs Prevent Replicative Stress in Response to Mitogenic Signaling
Bueno, M. J., de Cedrón, M. G., Laresgoiti, U., Fernández‐Piqueras, J., Zubiaga, A. M., & Malumbres, M. (2010) · Molecular and Cellular Biology · doi:10.1128/mcb.01372-09 · Cited by 103
“Most mitogenic pathways that control cell cycle entry regulate the induction of D-type cyclins and the subsequent activation of CDKs, the catalytic activity required for G1/S progression (48).”
BackgroundSelf-citationCyclin-dependent kinase 2 is an ideal target for ovary tumors with elevated cyclin E1 expression
Yang, L., Fang, D., Chen, H., Lu, Y.-Y., Dong, Z., Ding, H., Jing, Q., Su, S., & Huang, S. (2015) · Oncotarget · doi:10.18632/oncotarget.4600 · Cited by 100
“CCNE1 is abnormally expressed in various tumor types [11, 22].”
BackgroundCEP55 is a determinant of cell fate during perturbed mitosis in breast cancer
Kalimutho, M., Sinha, D., Jeffery, J., Nones, K., Srihari, S., Fernando, W., Duijf, P. H. G., Vennin, C., Raninga, P. V., Nanayakkara, D. M., et al. (2018) · EMBO Molecular Medicine · doi:10.15252/emmm.201708566 · Cited by 100
“…al, 1999; Hernando et al, 2001), but rather affected by CNAs; for example amplification of PLK1 (Strebhardt & Ullrich, 2006; Degenhardt & Lampkin, 2010), AuroraA (Zhou et al, 1998b; Wang et al, 2006), survivin (Altieri, 2003), cyclin B (Malumbres & Barbacid, 2009), and NEK2 (Hayward et al, 2004).”
BackgroundUbiquitin–proteasome system and the role of its inhibitors in cancer therapy
Aliabadi, F., Sohrabi, B., Mostafavi, E., Pazoki–Toroudi, H., & Webster, T. J. (2021) · Open Biology · doi:10.1098/rsob.200390 · Cited by 101
Proliferation and Apoptosis Pathways and Factors in Oral Squamous Cell Carcinoma
He, S., Chakraborty, R., & Ranganathan, S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23031562 · Cited by 102
“This causes the upregulation of D-type cyclin production which complex with cyclin dependent kinases (CDKs) 4 and 6 and partially inactivates retinoblastoma protein (RB) [42].”
BackgroundInfluentialRole of nanoparticles in enhancing chemotherapy efficacy for cancer treatment
Ghazal, H., Waqar, A., Yaseen, F., Shahid, M., Sultana, M., Tariq, M., Bashir, M. K., Tahseen, H., Raza, T., & Ahmad, F. (2024) · Next Materials · doi:10.1016/j.nxmate.2024.100128 · Cited by 102
Two-way communication between the metabolic and cell cycle machineries: the molecular basis
Kaplon, J., van Dam, L., & Peeper, D. S. (2015) · Cell Cycle · doi:10.1080/15384101.2015.1044172 · Cited by 102
Bao, Z., Jacobsen, D. M., & Young, M. A. (2011) · Structure · doi:10.1016/j.str.2011.02.016 · Cited by 99
“, 2001), and CDK2 represents a potential therapeutic target (Malumbres and Barbacid, 2009).”
Huang, J.-L., Ren, T., Cao, S., Zheng, S., Hu, X., Hu, Y., Li, L., Chen, J., Zheng, L., & Wang, Q. (2015) · Oncotarget · doi:10.18632/oncotarget.5667 · Cited by 98
“It has been well-defined that tumour-associated cell cycle defects are often mediated by the accumulation of cyclins (CCNs) and cyclin-dependent kinases (CDKs) complexes and reduced activity of cyclin-dependent kinase inhibitors (CDKIs)[23,24].”
Cyclin-dependent kinase 9 (CDK9) is a novel prognostic marker and therapeutic target in osteosarcoma
Ma, H., Seebacher, N. A., Hornicek, F. J., & Duan, Z. (2018) · EBioMedicine · doi:10.1016/j.ebiom.2018.12.022 · Cited by 98
Cell-Cycle-Targeting MicroRNAs as Therapeutic Tools against Refractory Cancers
Hydbring, P., Wang, Y., Fassl, A., Li, X., Matía, V., Otto, T., Choi, Y. J., Sweeney, K. E., Suski, J. M., Yin, H., et al. (2017) · Cancer Cell · doi:10.1016/j.ccell.2017.03.004 · Cited by 98
“Analyses of mouse genetic models revealed the requirement for specific cyclins and CDKs in development and maintenance of a wide array of tumor types (Malumbres and Barbacid, 2009).”
InfluentialMolecular targets and anticancer potential of sanguinarine—a benzophenanthridine alkaloid
Galadari, S., Rahman, A. U., Pallichankandy, S., & Thayyullathil, F. (2017) · Phytomedicine · doi:10.1016/j.phymed.2017.08.006 · Cited by 97
Niu, Y., Xu, J., & Sun, T. (2019) · Journal of Cancer · doi:10.7150/jca.32628 · Cited by 102
“The cyclin D-CDK4/6-INK4-Rb pathway is commonly dysregulated in a wide variety of human cancers, such as sarcoma, glioma, breast tumors, lymphoma, leukaemias and melanoma [27, 28].”
BackgroundElsayed, S. A., Badr, H. E., di Biase, A., & El‐Hendawy, A. M. (2021) · Journal of Inorganic Biochemistry · doi:10.1016/j.jinorgbio.2021.111549 · Cited by 97
Stein, C., Riedl, S., Rüthnick, D., Nötzold, R. R., & Bauer, U. (2012) · Nucleic Acids Research · doi:10.1093/nar/gks767 · Cited by 97
“Consistently with its target genes p21 and p16, which are tumor suppressors and frequently silenced in human cancer thereby allowing deregulation of CDK activity and enforcement of cell cycle progression (21), PRMT6 has been found to be overexpressed in certain malignancies.”
BackgroundSignaling pathways in breast cancer: Therapeutic targeting of the microenvironment
Kamdje, A. H. N., Etet, P. F. S., Vecchio, L., Jm, M., Krampera, M., & Lukong, K. E. (2014) · Cellular Signalling · doi:10.1016/j.cellsig.2014.07.034 · Cited by 98
Sun, Y., Wu, X., Cai, X., Song, M., Zheng, J., Pan, C., Qiu, P., Zhang, L., Zhou, S., Tang, Z., et al. (2016) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201500989 · Cited by 97
Chen, X., Liao, Y., Long, D., Yu, T., Shen, F., & Lin, X. (2017) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2017.2989 · Cited by 96
“Cdc2, also known as cyclin dependent kinase 1 (CDK1), controls the cell cycle entry from the G2 to the M phase and promotes the commencement of mitotic phase events (1), the abnormal activation of which directly causes aberrant cell proliferation, and malignant transformation and tumorigenesis in prostate cancer cells…”
Puangpraphant, S., Berhow, M. A., Vermillion, K. E., Potts, G., & de Mejı́a, E. G. (2011) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201100128 · Cited by 96
“This cyclin–CDK complex is regulated by CDK inhibitors such as p21 and p27 [45].”
BackgroundPatel, H., Abduljabbar, R. F., Lai, C., Periyasamy, M., Harrod, A., Gemma, C., Steel, J. H., Patel, N. R., Busonero, C., Jerjees, D. A., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-1104 · Cited by 99
“Surprisingly, genetic studies have indicated that cell-cycle CDKs, with the exception of CDK1, are not essential for most cell types (12, 13).”
miR‐10b*, a master inhibitor of the cell cycle, is down‐regulated in human breast tumours
Biagioni, F., Moshe, N. B. B., Fontemaggi, G., Canu, V., Mori, F., Antoniani, B., Benedetto, A. D., Santoro, R., Germoni, S., Angelis, F. D., et al. (2012) · EMBO Molecular Medicine · doi:10.1002/emmm.201201483 · Cited by 95
E2f8 mediates tumor suppression in postnatal liver development
Kent, L. N., Rakijas, J. B., Pandit, S. K., Westendorp, B., Chen, H.-Z., Huntington, J. T., Tang, X., Bae, S., Srivastava, A., Senapati, S., et al. (2016) · Journal of Clinical Investigation · doi:10.1172/jci85506 · Cited by 95
Cyclin B2 Overexpression in Human Hepatocellular Carcinoma is Associated with Poor Prognosis
Li, R., Jiang, X., Zhang, Y., Wang, S., Chen, X., Yu, X., Ma, J., & Huang, X. (2019) · Archives of Medical Research · doi:10.1016/j.arcmed.2019.03.003 · Cited by 95
Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension
Weiß, A., Neubauer, M. C., Yerabolu, D., Kojonazarov, B. K., Schlueter, B. C., Neubert, L., Jonigk, D. D., Baal, N., Ruppert, C., Dorfmüller, P., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-10135-x · Cited by 96
Cui, D., Dai, J., Keller, J. M., Mizokami, A., Xia, S., & Keller, E. T. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-0242 · Cited by 95
“Docetaxel-mediated inhibition ofmicrotubular depolymerization induces cell-cycle arrest at G2–Mphase, whereas inhibition of theNotch pathway results inG1–S arrest via decreased cyclin E expression (39).”
BackgroundCyclin-Dependent Kinases as Coregulators of Inflammatory Gene Expression
Schmitz, M. L., & Kracht, M. (2015) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2015.10.004 · Cited by 94
Yang, W., Cho, H., Shin, H., Chung, J., Kang, E. S., Lee, E., & Kim, J. (2016) · Oncotarget · doi:10.18632/oncotarget.10373 · Cited by 95
“Knockdown of Cdk1 increases G2/M arrest during the cell cycle and results in polyploid cells [1, 2, 4].”
BackgroundPhosphoregulation of the WAVE regulatory complex and signal integration
Mendoza, M. C. (2013) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2013.01.007 · Cited by 94
“Following nuclear envelope breakdown and cyclin A degradation, CDK1 is activated by Btype cyclins and promotes mitotic progression (reviewed in [68]).”
BackgroundLow Dose of Amino-Modified Nanoparticles Induces Cell Cycle Arrest
Kim, J. A., Åberg, C., de Cárcer, G., Malumbres, M., Salvati, A. L., & Dawson, K. A. (2013) · ACS Nano · doi:10.1021/nn403126e · Cited by 95
Self-citationCyclin-Dependent Kinase 2 Promotes Tumor Proliferation and Induces Radio Resistance in Glioblastoma
Wang, J., Yang, T., Xu, G., Liu, H., Ren, C., Xie, W., & Wang, M. (2016) · Translational Oncology · doi:10.1016/j.tranon.2016.08.007 · Cited by 94
“Discussion Accumulating data suggests that CDKs are targets of interest for anticancer drug development as uncontrolled activation of CDKs can accelerate tumor proliferation [15].”
The cell cycle checkpoint inhibitors in the treatment of leukemias
di Rorà, A. G. L., Iacobucci, I., & Martinelli, G. (2017) · Journal of Hematology & Oncology · doi:10.1186/s13045-017-0443-x · Cited by 95
“Although in normal cells the cell cycle checkpoint kinases as well as other elements of the DDR pathway act as tumor suppressor and are crucial for the maintenance of genetic stability, in cancer, they have been found to protect tumor cells from different stresses and, consequently, to promote tumor progression [37].”
BackgroundTranscription and Translation Inhibitors in Cancer Treatment
Laham-Karam, N., Pinto, G., Poso, A., & Kokkonen, P. (2020) · Frontiers in Chemistry · doi:10.3389/fchem.2020.00276 · Cited by 93
MiT/TFE Family of Transcription Factors: An Evolutionary Perspective
Spina, M. L., Contreras, P. S., Rissone, A., Meena, N. K., Jeong, E., & Martina, J. A. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.609683 · Cited by 92
“…et al., 2019 Myelinization repression Neurodegeneration Meireles et al., 2018 Regulation of cell cycle transition and proliferation Cell cycle Malumbres and Barbacid, 2009; Young et al., 2016; Doronzo et al., 2019; Kobayashi et al., 2019; Pastore et al., 2020; Pisonero-Vaquero et al., 2020;…”
BackgroundGatifloxacin Induces S and G2-Phase Cell Cycle Arrest in Pancreatic Cancer Cells via p21/p27/p53
Yadav, V., Sultana, S., Yadav, J., & Saini, N. (2012) · PLoS ONE · doi:10.1371/journal.pone.0047796 · Cited by 94
“Cyclin A, Cyclin E and CDK2 regulates normal S-phase progression [33;34] and we found Gatifloxacin to significantly decrease the expression levels of these proteins in both the cell lines in a dose dependent manner after 48 h (Figure 7A).”
BackgroundCDK4 Amplification Reduces Sensitivity to CDK4/6 Inhibition in Fusion-Positive Rhabdomyosarcoma
Olanich, M. E., Sun, W., Hewitt, S. M., Abdullaev, Z., Pack, S., & Barr, F. G. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-2955 · Cited by 96
“As one of three interphase CDKs that promote cell-cycle progression from G1 to S phase, CDK4 is a well-established protooncogene (11, 19).”
Metadata
- Authors
- Malumbres, M., & Barbacid, M.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Venue
- Nature Reviews Cancer
- Published
- 2009-03
- Volume
- 9
- Issue
- 3
- Pages
- 153-166
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2046024621
- Cited by
- 3,957
- References
- 178
- Citations by year
- 2026: 191 · 2025: 241 · 2024: 266 · 2023: 277 · 2022: 297 · 2021: 318 · 2020: 272 · 2019: 222 · 2018: 237 · 2017: 260 · 2016: 195 · 2015: 228 · 2014: 218 · 2013: 206 · 2012: 186
- FWCI
- 15.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- 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 › PI3K/AKT/mTOR signaling in cancer
- Keywords
- cyclin-dependent kinases, CDK1, cell cycle, tumor cell proliferation, genomic instability, chromosomal instability, cyclin-dependent kinase inhibitors, selective cancer therapy
- MeSH terms
- Animals, Cell Cycle, Chromosome Aberrations, DNA Damage, Humans, Mitosis, Neoplasms, Neoplastic Stem Cells, Cyclins, Cyclin-Dependent Kinases, Cyclin E, Chromosomal Instability, Protein Kinase Inhibitors, Cell Proliferation, Cyclin D
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