Importance of the stress kinase p38α in mediating the direct cytotoxic effects of the Thalidomide analogue, CPS49, in cancer cells and endothelial cells

Clinical Cancer Research

Volumn 12, Issue 11 I, 2006, Pages 3502-3509

  Warfel, Noel A ^a   Lepper, Erin R ^b   Zhang, Chunyu ^a   Figg, William D ^a   Dennis, Phillip A ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b SAIC FREDERICK INC   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

4 (4 FLUOROPHENYL) 2 (4 METHYLSULFINYLPHENYL) 5 (4 PYRIDYL)IMIDAZOLE; ALPHA TUBULIN; CPS 11; CPS 49; MITOGEN ACTIVATED PROTEIN KINASE; PHOSPHOTRANSFERASE; PHOSPHOTRANSFERASE INHIBITOR; STRESS KINASE P38ALPHA; SYNAPTOPHYSIN; THALIDOMIDE DERIVATIVE; UNCLASSIFIED DRUG; UO 126;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CANCER CELL; CANCER MODEL; CELL DEATH; CELL SURVIVAL; CONTROLLED STUDY; CYTOTOXICITY; DOSE RESPONSE; ENDOTHELIUM CELL; ENZYME ACTIVITY; HUMAN; HUMAN CELL; IMMUNOBLOTTING; IMMUNOHISTOCHEMISTRY; MOUSE; NONHUMAN; PRIORITY JOURNAL; XENOGRAFT;

ANIMALS; BUTADIENES; CELL DEATH; CELL LINE, TUMOR; CELL PROLIFERATION; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG SCREENING ASSAYS, ANTITUMOR; ENDOTHELIAL CELLS; ENZYME INHIBITORS; EXTRACELLULAR SIGNAL-REGULATED MAP KINASES; HUMANS; IMIDAZOLES; MICE; MICE, SCID; MITOGEN-ACTIVATED PROTEIN KINASE 14; NEOPLASMS; NITRILES; PYRIDINES; STRUCTURE-ACTIVITY RELATIONSHIP; THALIDOMIDE; XENOGRAFT MODEL ANTITUMOR ASSAYS;

EID: 33745214607     PISSN: 10780432     EISSN: None     Source Type: Journal    
DOI: 10.1158/1078-0432.CCR-05-1837     Document Type: Article

References (25)

1. Lenz W, Knapp K. Thalidomide embryopathy. Arch Environ Health 1962;5:100-5.
2. D'Amato RJ, Loughnan MS, Flynn E, Folkman J. Thalidomide is an inhibitor of angiogenesis. Proc Natl Acad Sci U S A 1994;91:4082-5.
3. Rajkumar SV, Fonseca R, Dispenzieri A, et al. Thalidomide in the treatment of relapsed multiple myeloma. Mayo Clin Proc 2000;75:897-901.
4. Kumar S, Gertz MA, Dispenzieri A, et al. Response rate, durability of response, and survival after thalidomide therapy for relapsed multiple myeloma. Mayo Clin Proc 2003;78:34-9.
5. Patt YZ, Hassan MM, Lozano RD, Ellis LM, Peterson JA, Waugh KA. Durable clinical response of refractory hepatocellular carcinoma to orally administered thalidomide. Am J Clin Oncol 2000;23:319-21.
6. Little RF, Wyvill KM, Pluda JM, et al. Activity of thalidomide in AIDS-related Kaposi's sarcoma. J Clin Oncol 2000;18:2593-602.
7. Figg WD, Dahut W, Duray P, et al. A randomized phase II trial of thalidomide, an angiogenesis inhibitor, in patients with androgen-independent prostate cancer. Clin Cancer Res 2001;7:1888-93.
8. Ng SS, MacPherson GR, Gutschow M, Eger K, Figg WD. Antitumor effects of thalidomide analogs in human prostate cancer xenografts implanted in immunodeficient mice. Clin Cancer Res 2004;10:4192-7.
9. Ando Y, Fuse E, Figg WD. Thalidomide metabolism by the CYP2C subfamily. Clin Cancer Res 2002;8: 1964-73.
10. Lepper ER, Ng SS, Gutschow M, et al. Comparative molecular field analysis and comparative molecular similarity indices analysis of thalidomide analogues as angiogenesis inhibitors. J Med Chem 2004; 47:2219-27.
11. Ng SS, Gutschow M, Weiss M, et al. Antiangiogenic activity of N-substituted and tetrafluorinated thalidomide analogues. Cancer Res 2003;63: 3189-94.
12. Brognard J, Clark AS, Ni Y, Dennis PA. Akt/protein kinase B is constitutively active in non-small cell lung cancer cells and promotes cellular survival and resistance to chemotherapy and radiation. Cancer Res 2001;61:3986-97.
13. Brognard J, Dennis PA. Variable apoptotic response of NSCLC cells to inhibition of the MEK/ERK pathway by small molecules or dominant negative mutants. Cell Death Differ 2002;9:893-904.
14. Dredge K, Marriott JB, Macdonald CD, et al. Novel thalidomide analogues display anti-angiogenic activity independently of immunomodulatory effects. Br J Cancer 2002;87:1166-72.
15. Clark AS, West K, Streicher S, Dennis PA. Constitutive and inducible Akt activity promotes resistance to chemotherapy, trastuzumab, or tamoxifen in breast cancer cells. Mol Cancer Ther 2002;1:707-17.
16. Kumar S, Raje N, Hideshima T, et al. Antimyeloma activity of two novel N-substituted and tetraflourinated thalidomide analogs. Leukemia 2005;19: 1253-61.
17. Berra E, Diaz-Meco MT, Moscat J. The activation of p38 and apoptosis by the inhibition of Erk is antagonized by the phosphoinositide 3-kinase/Akt pathway. J Biol Chem 1998;273:10792-7.
18. Johnson GL, Lapadat R. Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science 2002;298:1911-2.
19. Schieven GL. The biology of p38 kinase: a central role in inflammation. Curr Top Med Chem 2005;5: 921-8.
20. Olson JM, Hallahan AR. p38 MAP kinase: a convergence point in cancer therapy. Trends Mol Med 2004; 10:125-9.
21. Losa JH, Parada Cobo C, Viniegra JG, Sanchez-Arevalo Lobo VJ, Ramon y Cajal S, Sanchez-Prieto R. Role of the p38 MAPK pathway in cisplatin-based therapy. Oncogene 2003;22:3998-4006.
22. Habiro A, Tanno S, Koizumi K, et al. Involvement of p38 mitogen-activated protein kinase in gemcitabine-induced apoptosis in human pancreatic cancer cells. Biochem Biophys Res Commun 2004;316:71-7.
23. Kumar P, Miller AI, Polverini PJ. p38 MAPK mediates γ-irradiation- induced endothelial cell apoptosis, and vascular endothelial growth factor protects endothelial cells through the phosphoinositide 3-kinase-Akt-Bcl-2 pathway. J Biol Chem 2004;279:43352-60.
24. Issbrucker K, Marti HH, Hippenstiel S, et al. p38 MAP kinase-a molecular switch between VEGF-induced angiogenesis and vascular hyperpermeability. FASEB J 2003;17:262-4.
25. Greenberg AK, Basu S, Hu J, et al. Selective p38 activation in human non-small cell lung cancer. Am J Respir Cell Mol Biol 2002;26:558-64.