18
Views
10
CrossRef citations to date
0
Altmetric
Article

Androgen and the blocking of radiation‐induced sensitization to Fas‐mediated apoptosis through c‐jun induction in prostate cancer cells

, , , &
Pages 451-462 | Received 25 Nov 2002, Accepted 04 May 2003, Published online: 03 Jul 2009

References

  • ALBERTS, B., 1998, The cell as a collection of protein machines: preparing the next generation of molecular biologists. Cell, 92, 291–294.
  • ASHKENAZI, A. and Ducrr, V. M., 1998, Death receptors: signalling and modulation. Science, 281, 1305–1308.
  • BOLDEN, M. P., GONCHAROV, T. M., GOLTSEV, Y. V. and WALLACH, D., 1996, Involvement of MACH, a novel MORT1/ FADD-interacting protease, in Fas/APO-l- and TNF receptor-induced cell death. Cell, 85, 803–815.
  • BOLLA, M., GONZALEZ, D., WARDE, P., DUBOIS, J. B., MimmANOFF, R. 0., STORME, G., BERNIER, J., KUTEN, A., STERNBERG, C., GIL, T., COLLETTE, L. and PIERART, M., 1997, Improved survival in patients with locally advanced prostate cancer treated with radiotherapy and goserelin. New England Journal of Medicine, 337, 295–300.
  • BRANDSTROM, A., WESTIN, P., BERGH, A., CAJANDER, S. and DAMBER, J. E., 1994, Castration induces apoptosis in the ventral prostate but not in an androgen-sensitive prostatic adenocarcinoma in the rat. Cancer Research, 54, 3594–3601.
  • CANMAN, C. E., GnmEE, T. M., Courrs, S. B. and KASTAN, M. B., 1995, Growth factor modulation of p53-mediated growth arrest versus apoptosis. Genes and Development, 9, 600–611.
  • CARSON, J. P., KULIK, G. and WEBER, M. J., 1999, Antiapoptotic signalling in LNCaP prostate cancer cells: a survival signalling pathway independent of phosphatidylinositol 3'-kinase and Akt/protein kinase B. Cancer Research, 59, 1449–1453.
  • COLLETIER, P. J., ASHOORI, F., COWEN, D., ME, R. E., TOITLON, P., MEISTRICH, M. E. and POLLACK, A., 2000, Adenoviral-mediated p53 transgene expression sensitizes both wild-type and null p53 prostate cancer cells in vitro to radiation. International Journal Radiation Oncology, Biology, Physics, 48, 1507–1512.
  • COSTA-PEREIR AA. P., MCKENNA, S. L. and COTT'ER, T. G., 2000, Activation of SAPK/JNK by camptothecin sensitizes androgen-independent prostate cancer cells to Fas-induced apoptosis. British Journal of Cancer, 82, 1827–1834.
  • DEWEESE, T. L., SHIPMAN, J. M., DITIYHAY, L. E. and NELSON, W. G., 1998, Sensitivity of human prostatic carcinoma cell lines to low dose rate radiation exposure. Journal of Urology, 159, 591–598.
  • FUKAZAWA, T., FUJIWARA, T., UNO, F., TERAISHI, F., KADowmu, Y., ITOSHIMA, T., TAKATA, Y., KAGAWA, S., Rom, J. A., TSCHOPP, J. and TANAKA, N., 2001, Accelerated degradation of cellular FLIP protein through the ubiquitin-proteasome pathway in p53-mediated apoptosis of human cancer cells. Oncogene, 20, 5225–5231.
  • FULDA, S., MEYER, E. and DEBATIN, K. M., 2000, Metabolic inhi-bitors sensitize for CD95 (APO-1/Fas)-induced apoptosis by down-regulating Fas-associated death domain-like interleukin 1-converting enzyme inhibitory protein expres-sion. Cancer Research, 60, 3947–3956.
  • GEWIES, A., ROM-MIN, 0. W. and COHEN, M. B., 2000, Cytochrome c is involved in Fas-mediated apoptosis of prostatic carcinoma cell lines. Cancer Research, 60, 2163–2168.
  • HEDLUND, T. E., DuEE, R. C., SCHLEICHER, M. S. and MILLER, G. J., 1998, Fas-mediated apoptosis in seven human prostate cancer cell lines: correlation with tumor stage. Prostate, 36, 92–101.
  • HIROTA, Y., HORIUCHI, T. and AKAHANE, K., 1996, p53 antisense oligonucleotide inhibits growth of human colon tumor and normal cell lines. Japanese Journal of Cancer Research, 87, 735–742.
  • JIANG, J., ULBRIGHT, T. M., ZHANG, S., ECKERT, G. J., KAO, C., GARDNER, T. A., Kom, M. 0., EBLE, J. N. and CHENG, L., 2002, Fas and Fas ligand expression is elevated in prostatic intraepithelial neoplasia and prostatic adeno-carcinoma. Cancer, 95, 296–300.
  • KAzAmA, H. and YONEHARA, S., 2000, Oncogenic K-Ras and basic fibroblast growth factor prevent Fas-mediated apoptosis in fibroblasts through activation of mitogen-activated protein kinase. Journal of Cell Biology, 148, 557–566.
  • KIMURA, K., BOWEN, C., SPIEGEL, S. and GELMANN, E. P., 1999, Tumor necrosis factor-alpha sensitizes prostate cancer cells to gamma-irradiation-induced apoptosis. Cancer Research, 59, 1606–1614.
  • KusuEA, K. and GELMANN, E. P., 2002, Propapoptotic effects of NF-kappaB in LNCaP prostate cancer cells lead to serine protease activation. Cell Death and Dtffèrentiation, 9, 972–980.
  • KIMURA, K., MARKOWSKI, M., BOWEN, C. and GELmANN, E. P., 2001, Androgen blocks apoptosis of hormone-dependent prostate cancer cells. Cancer Research, 61, 5611–5618.
  • Ko, L. J. and PRIVES, C., 1996, p53: puzzle and paradigm. Genes and Development, 10, 1054–1072.
  • KoKoNns, J. M., HAY, N. and LIAO, S., 1998, Progression of LNCaP prostate tumor cells during androgen deprivation: hormone-independent growth, repression of proliferation by androgen, and role for p27Kip 1 in androgen-induced cell cycle arrest. Molecular Endocrinology, 12, 941–953.
  • KONDO, T., MATSUDA, T., KrrANo, T., TAEAHAsm, A., TASHIMA, M., IstrauEA, H., UMEHARA, H., DOMAE, N., UctuyAmA, T. and OKAZAIU, T., 2000, Role of c-jun expression increased by heat shock- and ceramide-activated caspase-3 in HL-60 cell apoptosis. Possible involvement of ceramide in heat shock-induced apoptosis. Journal of Biological Chemistry, 275, 7668–7676.
  • LEITH, J. T., 1994, In vitro radiation sensitivity of the LNCaP prostatic tumor cell line. Prostate, 24, 119–124.
  • Low, W., Smirru, A., ASHWORTH, A. and COLLINS, M., 1999, JNK activation is not required for Fas-mediated apoptosis. Oncogene, 18, 3737–3741.
  • Luo, R. X., POSTIGO, A. A. and DEAN, D. C., 1998, Rb interacts with histone deacetylase to repress transcription. Cell, 92, 463–473.
  • MESSING, E. M., MANOLA, J., SAROSDY, M., WILDING, G., CRAWFORD, E. D. and TRUMP, D., 1999, Immediate hormonal therapy compared with observation after radical prostatectomy and pelvic lymphadenectomy in men with node-positive prostate cancer. New England Journal of Medicine, 341, 1781–1788.
  • MULLER, M., WILDER, S., BANNASCH, D., ISRAELI, D., LEFILBACH, K., LI-WEBER, M., FRIEDMAN, S. L., GALLE, P. R., STREMMEL, W., OR, M. and KRAmmER, P. H., 1998, p53 activates the CD95 (APO-1/Fas) gene in response to DNA damage by anticancer drugs. Journal of Experimental Medicine, 188, 2033–2045.
  • NAGATA, S., 1997, Apoptosis by death factor. Cell, 88, 355-365. NAGATA, S. and GOLSTEIN, P., 1995, The Fas death factor. Science, 267, 1449–1456.
  • NEWTON, K. and STRASSER, A., 2000, Ionizing radiation and chemotherapeutic drugs induce apoptosis in lymphocytes in the absence of Fas or FADD/MORT1 signalling. Implications for cancer therapy. Journal of Experimental Medicine, 191, 195–200.
  • OHYAMA, T., Tsuxumo, S., YAJImA, N., SAKAmmu, K. and YONEHARA, S., 2000, Reduction of thymocyte numbers in transgenic mice expressing viral FLICE-inhibitory protein in a Fas-independent manner. Microbiology Immunology, 44, 289–297.
  • PFLUG, B. R., RErrER, R. E. and NELSON, J. B., 1999, Caveolin expression is decreased following androgen deprivation in human prostate cancer cell lines. Prostate, 40, 269–273.
  • POLLACK, A., SALEM, N., ASHOORI, F., HACHEM, P., SANGHA, M., VON ESCHENBACH, A. C. and MEISTRICH, M. L., 2001, Lack of prostate cancer racliosensitization by androgen depri-vation. International Journal of Radiation Oncology Biology Physics, 51, 1002–1007.
  • Roximmr, 0. W., BISHOP, G. A., HOSTAGER, B. S., WALDSCHMIDT, T. J., SIDORENKO, S. P., PAVLOFF, N., KIEFER, M. C., UMANSKY, S. R., GLOVER, R. A. and COHEN, M. B., 1997, Fas-mediated apoptosis in human prostatic carcinoma cell lines. Cancer Research, 57, 1758–1768.
  • Roximmr, 0. W., GLOVER, R. A. and COHEN, M. B., 1998, Fas-mediated apoptosis in human prostatic carcinoma cell lines occurs via activation of caspase-8 and caspase-7. Cancer Research, 58, 5870–5875.
  • SHAULIAN, E. and KARIN, M., 2001, AP-1 in cell proliferation and survival. Oncogene, 20, 2390–2400.
  • SHAULIAN, E., SCHREIBER, M., Pm, F., BEECHE, M., WAGNER, E. F. and KARIN, M., 2000, The mammalian UV response: c-Jun induction is required for exit from p53-imposed growth arrest. Cell, 103, 897–907.
  • SFIIMADA, K., NAKAMURA, M., ISHEDA, E., KISHI, M., YONEHARA, S. and Komsm, N., 2003a, c-Jun NH2-terminal kinase-dependent Fas activation contributes to etoposide-induced apoptosis in p53-mutated prostate cancer cells. Prostate, 55, 265–280.
  • SFIIMADA, K., NAKAMURA, M., ISHEDA, E., KISHI, M., YONEHARA, S. and Komsm, N., 2002a, Contributions of mitogen-activated protein kinase and nuclear factor kappa B to N-(4-hydroxyphenyl)retinamide-induced apoptosis in prostate cancer cells. Molecular Carcinogenesis, 35, 127–137.
  • SFIIMADA, K., NAKAMURA, M., ISFIEDA, E., KISHI, M., YONEHARA, S. and Komsm, N., 2002b, Phosphorylation of Fas-associated death domain contributes to enhancement of etoposide-induced apoptosis in prostate cancer cells. Japanese Journal of Cancer Research, 93, 1164–1174.
  • SHIMADA, K., NAKAMURA, M., ISHIDA, E., KISHI, M., YONEHARA, S. and Komsm, N., 2003b, The requirement of c-jun for testosterone-induced sensitization to N-(4-hydroxyphenyl) retinamide-induced apoptosis. Molecular Carcinogenesis, 36, 115–122.
  • Suzum, A., MATSUZAWA, A. and IGucm, T., 1996, Down regulation of Bc1-2 is the first step on Fas-mediated apoptosis of male reproductive tract. Oncogene, 13, 31–37.
  • Suzum, A., Tsuromi, Y., AKAHANE, K., ARAKI, T. and MIURA, M., 1998, Resistance to Fas-mediated apoptosis: activation of caspase 3 is regulated by cell cycle regulator p21WAF1 and IAP gene family ILP. Oncogene, 17, 931–939.
  • TAKAYAMA, H., TAKAKUWA, T., DONG, Z., NONOMURA, N., OKUYAMA, A., NAGATA, S. and AOZASA, K., 2001, Fas gene mutations in prostatic intraepithelial neoplasia and concurrent carcinoma: analysis of laser capture microdissected specimens. Laboratory Investigation, 81, 283–288.
  • TAKESHITA, A., WATANABE, A., TAKADA, Y. and HANAZAWA, S., 2000, Selective stimulation by ceramide of the expression of the alpha isoform of retinoic acid and retinoid X receptors in osteoblastic cells. A role of sphingosine 1-phosphate-mediated AP-1 in the ligand-dependent transcriptional activity of these receptors. Journal of Biological Chemistry, 275, 32220–32226.
  • TAKEucm, T., SAsAxr, Y., UEIU, T., KAziwARA, T., MOIUYAMA, N., KmATARE, K. and KAKIZOE, T., 1996, Modulation of growth and apoptosis response in PC-3 and LNCAP prostate-cancer cell lines by Fas. International Journal of Cancer, 67, 709–714.
  • WRIGHT, P. S., CROSS-DOERSEN, D., TH'NG, J. P., Guo, X. W., CRISSMAN, H. A., BRADBURY, E. M., MONTGOMERY, L. R., THOMPSON, F. Y., LouDY, D. E., JOHNSTON, J. 0. and BrroNTI, A. J., 1996, A ribonucleotide reductase inhibitor, MDL 101,731, induces apoptosis and elevates TRPM-2 mRNA levels in human prostate tumor xenografts. Experimental Cell Research, 222, 54–60.
  • YONEHARA, S., 1999, Effects of anti-Fas antibodies on lymphocytes and other organs: preparation of original and new monoclonal antibodies and amelioration of systemic autoimmune disease. International Review of Immunology, 18, 329–345.
  • YuAN, X. J. and WHANG, Y. E., 2002, PTEN sensitizes prostate cancer cells to death receptor-mediated and drug-induced apoptosis through a FADD-dependent pathway. Oncogene, 21, 319–327.
  • ZHANG, S., ZENG, G., KAO, C., GARDNER, T., SWEENEY, C., YANG, N. S., EBLE, J. N. and CHENG, L., 2002, Fas-Fas ligand signalling pathway mediates an interleukin-12-induced rejection of a murine prostate tumor system. Prostate, 53, 69–76.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.