The cell cycle, chromatin and cancer: Mechanism-based therapeutics come of age

Drug Discovery Today

Volumn 8, Issue 17, 2003, Pages 793-802

  McLaughlin, Fiona ^a   Finn, Paul ^a   La Thangue, Nicholas B ^a,b  

^a BioAlliance Pharma   (France)

^b UNIVERSITY OF GLASGOW   (United Kingdom)

Author keywords

Cancer biology; Cell biology; Cell cycle; Checkpoints; Chromatin; Cyclin dependent kinases; Drug Discovery; Histone deacetylase; Pharmaceutical Science

Indexed keywords

3 PHENYLSULFAMOYLCINNAMOHYDROXAMIC ACID; 4 [N (2 HYDROXYETHYL) N [2 (3 INDOLYL)ETHYL]AMINOMETHYL]CINNAMOHYDROXAMIC ACID; 7 HYDROXYSTAUROSPORINE; ANTINEOPLASTIC AGENT; CISPLATIN; CYCLIN DEPENDENT KINASE INHIBITOR; CYCLOPHOSPHAMIDE; DOXORUBICIN; FLAVOPIRIDOL; FR 901228; GW 491619; METHOTREXATE; OXINDOLE; PACLITAXEL; PHOSPHATIDYLINOSITOL 3 KINASE; RETINOBLASTOMA PROTEIN; ROSCOVITINE; SB 218078; STAUROSPORINE DERIVATIVE; UNCLASSIFIED DRUG; VORINOSTAT;

CANCER; CANCER CELL; CANCER CHEMOTHERAPY; CANCER CLASSIFICATION; CANCER MORTALITY; CANCER SURVIVAL; CELL CYCLE; CELL CYCLE G1 PHASE; CELL CYCLE S PHASE; CELL PROLIFERATION; CELL TRANSFORMATION; CHILDHOOD LEUKEMIA; CHROMATIN STRUCTURE; DNA STRAND BREAKAGE; DRUG IDENTIFICATION; GASTROINTESTINAL TOXICITY; GENE TARGETING; HUMAN; HYPERGLYCEMIA; HYPOTENSION; LUNG CARCINOMA; LUNG DISEASE; PROTEIN PHOSPHORYLATION; REVIEW; SURVIVAL RATE; SURVIVAL TIME; TARGET CELL DESTRUCTION; TESTIS CANCER;

ANIMALS; ANTINEOPLASTIC AGENTS; CELL CYCLE; CHROMATIN; CYCLIN-DEPENDENT KINASES; DRUG DELIVERY SYSTEMS; HISTONE DEACETYLASES; HUMANS; NEOPLASMS;

EID: 0042933857     PISSN: 13596446     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1359-6446(03)02792-2     Document Type: Review

References (67)

1. Sherr C.J., Roberts J.M. CDK inhibitors: positive and negative regulators of G1-phase progression. Genes Dev. 13:1999;1501-1512.
2. Dyson N. The regulation of E2F by pRb-family proteins. Genes Dev. 12:1998;2245-2262.
3. Zhou B.-B., Elledge S.J. The DNA damage response: putting checkpoints in perspective. Nature. 408:2000;433-439.
4. Khanna K.K., Jackson S.P. DNA double-strand breaks: repair and the cancer connection. Nat. Genet. 27:2001;247-254.
5. Stevens C., La Thangue N.B. E2F and cell cycle control: a double-edged sword. Arch. Biochem. Biophys. 412:2003;157-169.
6. Brooks G., La Thangue N.B. The cell cycle and drug discovery: the promise and the hope. Drug Discov. Today. 4:1999;455-464.
7. Workman P., Kaye S. A trends guide to cancer therapeutics. Trends Mol. Med. 8:(Suppl):2002;S1-S9.
8. Meijer L., et al. Progress in Cell Cycle Research: Cell Cycle Regulators as Therapeutic Targets. 2003;Kluwer.
9. La Thangue N.B., Bandara L.R. Targets for Cancer Chemotherapy: Transcription factors and Other Nuclear Proteins. 2002;Humana Press.
10. Gali-Muhtasib H., Bakkar N. Modulating cell cycle: current applications and prospects for future drug development. Curr. Cancer Drug Targets. 4:2002;309-336.
11. st Century. A Vision for All. World Health Organisation, Geneva Switzerland.
12. On the World Wide Web URL http://www.cancerresearchuk.org/aboutcancer/statistics.
13. Hanahan D., Weinberg A. The hallmarks of cancer. Cell. 100:2000;57-70.
14. Sherr C.J. Cancer cell cycles. Science. 274:1996;1672-1677.
15. Peng C.-Y., et al. Mitotic and G2 checkpoint control: regulation of 14-3-3 binding by phosphorylation of Cdc25C on serine 216. Science. 277:1997;1501-1505.
16. Hirao A., et al. DNA damage induced activation of p53 by checkpoint kinase chk2. Science. 287:2002;1824-1827.
17. Stevens C., et al. Chk2 activates E2F-1 in response to DNA damage. Nat. Cell Biol. 5:2003;401-409.
18. Bartek J., et al. Chk2 kinase: A busy inhibitor. Nat. Rev. Mol. Cell Biol. 2:2001;877-886.
19. Kouzarides T. Histone acetylases in cell proliferation. Curr. Opin. Dev. 9:1999;40-48.
20. Strahl B.D., Allis C.D. The language of covalent histone modifications. Nature. 403:2000;41-45.
21. Jenuwein T., Allis C.D. Translating the histone code. Science. 293:2001;1074-1080.
22. Chan H.-M., La Thangue N.B. p300/CBP proteins: HATS for transcriptional bridges and scaffolds. J. Cell Sci. 114:2001;2363-2373.
23. Hsueh C.-T., et al. UCN-01 suppresses thymidylate synthase gene expression and enhances 5-fluorouracil-induced apoptosis in a sequence-dependent manner. Clin. Cancer Res. 4:1998;2201-2206.
24. Thomas J.P., et al. Phase I clinical and pharmacokinetic trial of the cyclin-dependent kinase inhibitor flavopiridol. Cancer Chemother. Pharmacol. 50:2002;465-472.
25. Akiyama T., et al. G1 phase accumulation induced by UCN-01 is associated with dephosphorylation of Rb and CDK2 proteins as well as induction of CDK inhibitor p21/Cip1/WAF1/Sdi 1 in p53-mutated human epidermoid carcinoma A431 cells. Cancer Res. 576:1997;1495-1501.
26. Wang Q., et al. UCN-01, a potent abrogator of G2 checkpoint function in cancer cells with disrupted p53. J. Natl. Cancer Inst. 88:1996;956-965.
27. Wadler S. Perspectives for cancer therapies with Cdk2 inhibitors. Drug Resist. Updat. 4:2001;347-367.
28. Sausville E.A., et al. Phase 1 trial of 72hour continuous infusion UCN01 in patients with refractory neoplasms. J. Clin. Oncol. 15:2001;2319-2333.
29. Chao S.-H., Price D.H. Flavopiridol inactivates P-TEFb and blocks most RNA polymerase II transcription in vivo. J. Biol. Chem. 276:2001;31793-31799.
30. Fischer P.M. Recent advances and new directions in the discovery and development of cyclin-dependent kinase inhibitors. Curr. Opin. Drug Discov. 4:2001;623-634.
31. McClue S.J., et al. In vitro and in vivo anti-tumour properties of the cyclin-dependent kinase inhibitor CYC202 (R-Roscovitine). Int. J. Cancer. 102:2002;463-468.
32. Raymond E., et al. Preliminary results of an ongoing phase I and pharmacokinetic study of CYC202, a novel oral cyclin-dependent kinases inhibitor, in patients with advanced malignancies. Eur. J. Cancer. 38:(Suppl. 7):2002;S49. Abstract.
33. Knick, V.B. et al. (2000) Novel substituted oxindole inhibitors of cyclin-dependent kinases arrest an protect normal cells from chemotherapy induced toxicity in vitro. Proc. Am. Assoc. Cancer Res. 41 (Abstract).
34. Honma T., et al. A novel approach for the development of selective cdk4 inhibitors: library design based on locations of cdk4 specific amino acid residues. J. Med. Chem. 44:2001;4628-4640.
35. Chen Y.-N., et al. Selective killing of transformed cells by cyclin/cyclin-dependent kinase 2 agonists. Proc. Natl. Acad. Sci. U. S. A. 96:1999;4325-4329.
36. Mendoza N., et al. Selective cyclin-dependent kinase2/cyclin A antagonists that differ from ATP site inhibitors block tumour growth. Cancer Res. 63:2003;1020-1024.
37. Sharma S.K., et al. Identification of E2F-1 cyclin A antagonists. Bioorg. Med. Chem. Lett. 11:2001;2449-2452.
38. Hall-Jackson C.A., et al. ATR is a caffeine-sensitive, DNA-activated protein kinase with a substrate specificity distinct from DNA-PK. Oncogene. 18:1999;6707-6713.
39. Sarkaria J.N., et al. Inhibition of ATM and ATR kinase activites by the radiosensitizing agent, caffeine. Cancer Res. 59:1999;4375-4382.
40. Busby E.C., et al. The radiosensitizing agent 7-hydroxystaurosporine (UCN-01) inhibits the DNA damage checkpoint kinase hChk1. Cancer Res. 60:2000;2108-2112.
41. Graves P.R., et al. The Chk1 protein kinase and the Cdc25C regulatory pathways are targets of the anticancer agent UCN-01. J. Biol. Chem. 275:2000;5600-5605.
42. Yuichi H., et al. Abrogation of the Chk1-mediated G2 checkpoint pathway potentiates temozolomide-induced toxicity in a p53-independent manner in human glioblastoma cells. Cancer Res. 61:2001;5843-5849.
43. Jackson J.R., et al. An inhibitor of human checkpoint kinase (Chk1) abrogates cell cycle arrest caused by DNA damage. Cancer Res. 60:2000;566-572.
44. Westphal C.H., et al. ATM and p53 co-operate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity. Nat. Genet. 16:1997;397-401.
45. Komarov P.G., et al. A chemical inhibitor of p53 that protects mice from the side effects of cancer therapy. Science. 285:1999;1135-1138.
46. Gray S.G., Ekstrom T.J. The human histone deacetylase family. Exp. Cell Res. 262:2001;75-83.
47. Marks P.A., et al. Histone deacetylase inhibitors: inducers of differentiation or apoptosis of transformed cells. J. Natl. Cancer Inst. 92:2000;1210-1216.
48. Marks P.A., et al. Inhibitors of histone deacetylase are potentially effective anticancer agents. Clin. Cancer Res. 7:2001;759-760.
49. Richon V.M., et al. A class of hybrid polar inducers of transformed cell differentiation inhibits histone deacetylases. Proc. Natl. Acad. Sci. U. S. A. 95:1998;3003-3007.
50. Richon V.M., et al. Histone deacetylase inhibitors: development of suberoylanilide hydroxamic acid (SAHA) for the treatment of cancers. Blood Cells Mol. Dis. 27:2001;260-264.
51. Finnin M.S., et al. Structures of a histone deacetylase homologue bound to the TSA and SAHA inhibitors. Nature. 401:1999;188-193.
52. Sgouros G., et al. Synergistic interaction of suberoylanilide hydroxamic acid (SAHA) and radiation in human prostate tumour spheroids. Proc. Am. Soc. Clin. Oncol. 2:2002;105.
53. Almenara J., et al. Synergistic induction of mitochondrial damage and apoptosis in human leukaemia cells by flavopiridol and the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA). Leukaemia. 16:2002;1331-1343.
54. Budillon, A. et al. (2002) Growth arrest, apoptosis and potentiation of 5-fluorouracil and Raltitrexed cytotoxic effect induced by histone deacetylase inhibitor SAHA in colorectal cancer cells AACR NCI EORTC. Mol. Targets Cancer Ther. Abstr. 81 (Abstract).
55. Richon V.M., et al. Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene-associated histone acetylation. Proc. Natl. Acad. Sci. U. S. A. 97:2000;10014-10019.
56. Ferreira R., et al. Cell cycle-dependent recruitment of HDAC-1 correlates with deacetylation of histone H4 on an Rb-E2F target promoter. EMBO Rep. 2:2001;794-799.
57. Lin R.J., et al. Role of the histone deacetylase complex in acute promyelocytic leukaemia. Nature. 391:1998;811-814.
58. He L.Z., et al. Distinct interactions of PML-RARalpha and PLZF-RARalpha with co-repressors determine differential responses to RA in APL. Nat. Genet. 18:1998;126-135.
59. Grigani F., et al. Fusion proteins of the retinoic acid receptor-alpha recruit histone deacetylase in promyelocytic leukaemia. Nature. 391:1998;815-818.
60. He L.Z., et al. Histone deacetylase inhibitors induce remission in transgenic models of therapy-resistant acute promyelocytic leukaemia. J. Clin. Invest. 108:2001;1277-1278.
61. Minucci S., et al. Histone deacetylases: a common molecular target for differentiation treatment of acute myeloid leukaemias? Oncogene. 20:2001;3110-3115.
62. Plumb, J. et al. Inhibition of human tumour cell growth by the novel histone deacetylase inhibitor PXD101. Mol. Cancer Ther. (in press).
63. Remiszewski S., et al. Preclinical efficacy, toxicology and pharmacokinetics of NVP-LAQ824, a novel synthetic histone deacetylase inhibitor. Eur. J. Cancer. 38:(Supplement 7):2002;S99.
64. Piekarz R.L., et al. Inhibitor of histone deacetylation, depsipeptide (FR901228), in the treatment of peripheral and cutaneous T-cell lymphoma: a case report. Blood. 1:2001;2865-2868.
65. Bruner R.J., et al. Phase I trial of the histone deacetylase inhibitor depsipeptide (FR901228) in fludarabine refractory chronic lymphocytic leukaemia. Blood. 100:2002;1492. (Abstract).
66. Glasner, K. et al. (2002) Characteristics of novel non-hydroxymate inhibitors of histone deacetylases. AACR NCI EORT. Mol. Targets Cancer Ther. Abstr. 333 (Abstract).
67. Wong J.C., et al. Structural biasing elements for in-cell histone deacetylase paralog selectivity. J. Am. Chem. Soc. 125:2003;5586-5587.