Antitumor activity of a novel bis-aziridinylnaphthoquinone (AZ4) mediating cell cycle arrest and apoptosis in non-small cell lung cancer cell line NCI-H460

Acta Pharmacologica Sinica

Volumn 28, Issue 4, 2007, Pages 559-566

  Shyu, Kou Gea ^a   Huang, Sheng Tung ^b   Kuo, Hsien Shou ^c   Cheng, Wen Pin ^c   Lin, Yuh Ling ^d  

^a SHIN KONG WU HO SU MEMORIAL HOSPITAL   (Taiwan)

^b NATIONAL TAIPEI UNIVERSITY OF TECHNOLOGY   (Taiwan)

^c TAIPEI MEDICAL UNIVERSITY   (Taiwan)

^d FU JEN CATHOLIC UNIVERSITY   (Taiwan)

Author keywords

Apoptosis; Aziridinylnaphthoquinone; Bcl 2 protein; Cell cycle

Indexed keywords

ANTINEOPLASTIC AGENT; AZIRIDINYLNAPHTHOQUINONE; CASPASE 3; CASPASE 8; CASPASE 9; CELL CYCLE PROTEIN; CELL CYCLE PROTEIN 2; CYCLIN B; PROTEIN BCL 2; PROTEIN P21; PROTEIN P53; UNCLASSIFIED DRUG;

ANTINEOPLASTIC ACTIVITY; APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CELL CYCLE ARREST; CELL CYCLE G2 PHASE; CELL PROLIFERATION; CELL VIABILITY; CONTROLLED STUDY; CYTOTOXICITY; DOWN REGULATION; DRUG STRUCTURE; FLUORESCENCE ACTIVATED CELL SORTING; GROWTH DISORDER; HUMAN; HUMAN CELL; IC 50; LUNG NON SMALL CELL CANCER; PROTEIN EXPRESSION; UPREGULATION; WESTERN BLOTTING;

ANTINEOPLASTIC AGENTS; APOPTOSIS; CARCINOMA, NON-SMALL-CELL LUNG; CASPASES; CELL CYCLE; CELL LINE, TUMOR; G2 PHASE; HUMANS; LUNG NEOPLASMS; NAPHTHOQUINONES; PROTO-ONCOGENE PROTEINS C-BCL-2; TUMOR SUPPRESSOR PROTEIN P53;

EID: 33947704074     PISSN: 16714083     EISSN: 17457254     Source Type: Journal    
DOI: 10.1111/j.1745-7254.2007.00508.x     Document Type: Article

References (30)

1. Pakunlu RI, Wang Y, Tsao W, Pozharov V, Cook TJ, Minko T. Enhancement of the efficacy of chemotherapy for lung cancer by simultaneous suppression of multidrug resistance and antiapoptic cellular defense: novel multicomponent delivery system. Cancer Res 2004; 64: 6214-24.
2. Brown JM. Tumor microenvironment and the response to anticancer therapy. Cancer Biol Ther 2002; 1: 453-8.
3. Shannon AM, Bouchier-Hayes DJ, Condron CM, Toomey D. Tumor hypoxia, chemotherapeutic resistance and hypoxia-related therapies. Cancer Treat Rev 2003; 29: 297-307.
4. Naylor MA, Thomson P. Recent advances in bioreductive drug targeting. Mini-Rev Med Chem 2001; 1: 17-29.
5. Phillips RM, Burger AM, Loadman PM, Jarrett CM, Swaine DJ, Fiebig HH. Predicting tumor responses to mitomycine C on the basis of DT-diaphorase activity or drug metabolism by tumorhomogenares: implications for enzyme-directed bioreductive drug development. Cancer Res 2000; 60: 6384-90.
6. Kim JY, Kim CH, Stratford IJ, Patterson AV, Hendry JH. The bioreductive agents RH1 and gamma-irradiation both cause G2/ M cell cycle phase arrest and polyploidy in a p53-mutated human breast cancer cell line. Int J Rad Oncol Biol Phys 2004; 58: 376-58.
7. Siim BG, Pruijn FB, Sturman JR, Hogg A, Hay MP, Brown JM, et al. Selective potentiation of hypoxic cytotoxicity of tirapazamine by its 1-N-oxide metabolite SR4317. Cancer Res 2004; 62: 736-42.
8. Lin PS, Ho KC, Yang SJ. Tirapazamine (SR4233) interrupts cell cycle progression and induces apoptosis. Cancer Lett 1996; 105: 249-55.
9. Lee AE, Wilson WR. Hypoxia-dependent retinal toxicity of bioreductive anticancer prodrugs in mice. Toxicol App Pharmacol 2000; 163: 50-9.
10. Smitskamp-Wilms E, Giaccone G, Pinedo HM, Laan BFAM, Peters GJ. DT-diaphorase activity in normal and neoplastic human tissues; an indicator for sensitivity to bioreductive agents? Br J Cancer 1995; 72: 917-21.
11. Danson S, Ward TH, Butler J, Ranson M. DT-diaphorase: a target for new anticancer drugs. Cancer Treat Rev 2004; 30: 437-49.
12. Workman P, Walton MI. Enzyme directed bioreductive drug development. In: Fielden EM, Wardman P, editors. Selective activation of drug by redox processes. New York: Plenum Press; 1990. p173-91.
13. Huang ST, Kuo HS, Lin CM, Tsai HD, Peng YC, Chen CT, et al. Synthesis and biological evaluation of novel bis-aziridinylnaphthoquinone derivatives. Oncology Res 2003; 11: 199-204.
14. Skehan P, Storeng R, Scudiero D, Monks A, McMahon J, Vistica D, et al. New colorimetric cytotoxicity assay for anticancerdrug screening. J Natl Cancer Inst 1990; 82: 1107-12.
15. Komoriya A, Packard BZ, Brown MJ, Wu ML, Henkar PA. Assessment of caspase activities in intact apoptotic thymocytes using cell-permeable fluorogenic caspase substrates. J Exp Med 2000; 191: 1819-28.
16. Bacus SS, Gudkov AV, Lowe M, Lyass L, Yung Y. Taxol-induced apoptosis depends on MAP kinase pathways (ERK and p38) and is independent of p53. Oncogen 2001; 20: 147-55.
17. Dive C, Gregory CD, Phipps DJ, Evans DL, Miliner AE, Wyllic AL. Analysis and discrimination of necrosis and apoptosis (programmed cell death) by multiparameter flow cytometry. Biochim Biophys Acta 1992; 1133: 275-81.
18. Scheer M, Kuebler AC, Zoller JE. Chemoprevention of oral squamous cell carcinomas. Onkologie 2004; 27: 187-93.
19. Hsu S, Singh B, Schuster G. Induction of apoptosis in oral cancer cells: agents and mechanisms for potential therapy and prevention. Oral Oncol 2004; 40: 461-73.
20. Koontongkaew S, Chareonkitkajorn L, Chanvitan A, Leelakriangsak M, Amornphimolttham P. Alteration of p53, pRb, cyclin D (1) and cdk4 in human oral and pharyngeal squamous cell carcinomas. Oral Oncol 2000; 36: 334-9.
21. Schmitt CA, Low SW. Apoptosis and therapy. J Pathol 1999; 197: 127-37.
22. Evans GL, Vousden KH. Proliferation, cell cycle and apoptosis in cancer. Nature 2001; 411: 342-8.
23. Pirollo KF, Bouker KB, Chang EH. Does p53 status influence tumor response to anticancer therapies? Anti-cancer Drugs 2000; 11: 419-32.
24. Nylader K, Dabelsteen E, Hall PA. The p53 molecular and its prognostic role in squamous cell carcinomas of the head and neck. J Oral Pathol Med 2000; 29: 413-25.
25. Kaul R, Mukherjee S, Ahmed F, Bhat MK, Chhipa R, Galande S, et al. Direct interaction with and activation of p53 by SMAR1 retards cell-cycle progression at G2/M phase and delays tumor growth in mice. Int J Cancer 2003; 103: 606-15.
26. Gartel AL, Feliciano IL, Tyner A. A new method for determining the status of p53 in tumor cell lines of different origin. Oncol Res 2003; 13: 405-8.
27. Nikitakis NG, Sauk JJ, Papanicolaou SI. The role of apoptosis in oral disease: Mechanisms; aberrations in neoplastic, autoimmune, infectious, hematologic, and developmental diseases; and thera peutic opportunities. Oral Surg Oral Med Oral Pathol Oral Radiol & Endodo 2004; 97: 476-90.
28. Gibson LF, Fortney J, Magro G, Ericoson SG, Lynch JP, Landreth KS. Regulation of BAX and BCL-2 expression in breast cancer cells by chemotherapy. Breast Cancer Res Treat 1999; 55: 107-17.
29. Yamamoto K, Ichijo H, Korsmeyer SJ. BCL-2 is phosphorylated and inactivated by an ASK1/Jun N-terminal protein kinase pathway normally activated at G2/M. Mol Cell Biol 1999; 19: 8469-78.
30. Karl A, Nath KA. Provenance of the protective property of p21. Am J Physiol Renal Physiol 2005; 289: F512-3.