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研究生:許惠紋
研究生(外文):Hui-Wen Hsu
論文名稱:硫蜂斗菜素及其同分異構物對人類前列腺癌細胞之毒理效應
論文名稱(外文):Cytotoxic Effect of S-peptasin and Iso-S-peptasin on the Growth of Human Prostate Cancer Cells
指導教授:王錫崗王錫崗引用關係
指導教授(外文):Paulus Shyi-Gang Wang
學位類別:碩士
校院名稱:國立陽明大學
系所名稱:生理學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2004
畢業學年度:92
語文別:中文
論文頁數:92
中文關鍵詞:硫蜂斗菜素前列腺癌細胞細胞凋亡
外文關鍵詞:S-petasinProstate cancerApoptosis
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硫蜂斗菜素及異硫蜂斗菜素是由Petasites hybridus的根或葉萃取出來且具有生物活性的成份。Petasites hybridus在古希臘歷史中常用來治療胃腸道的和氣喘。此植物體及其萃取物應用在治療使用上已約有兩千年的歷史,在1994年的研究中指出其粹取物對於人類膀胱癌細胞株(T24)具有抗增殖的效果,且於2000年,本實驗室研究發現其粹取物-硫蜂斗菜素具有抑制大鼠間質細胞分泌睪固酮的效用,然而它對於人類前列腺癌細胞株是否也會造成毒殺效應,目前則尚未有文獻探討。前列腺癌早已成為美國男性最普遍的癌症之一,在台灣,近十年來男性罹患前列腺癌的發生率及死亡率亦逐年增高。在本篇論文研究當中,我選用了三種人類前列腺癌細胞株:LNCaP、DU145以及PC3作為研究對象,探討硫蜂斗菜素及異硫蜂斗菜素對於人類前列腺癌細胞株的抗增殖效應以及其作用機轉,研究過程中所使用的方法分別有:MTT細胞增殖分析法、錐蟲藍染色法、細胞倍增時間計算、光學顯微鏡攝影以及西方墨漬分析法。經由分析細胞增殖及細胞數量變化之後,發現硫蜂斗菜素及異硫蜂斗菜素可以有效的減少細胞數量,若同時以倒立式相位差顯微鏡觀察細胞型態之變化,可發現經過硫蜂斗菜素及異硫蜂斗菜素的刺激,可造成DU145及PC3細胞萎縮、並且有圓起、漂浮的現象,但在LNCaP細胞株中,僅能觀察到細胞有圓起、漂浮的現象,並沒有呈現明顯的萎縮。再以西方墨漬分析法分析與細胞凋亡相關的蛋白質,結果顯示,三種細胞株內的caspase 8、9、3均有被活化的現象,但caspase 7僅在LNCaP及PC3細胞中明顯被活化;此外,三種細胞之細胞質中的cytochrome c蛋白表現量也均因為藥物的刺激而明顯的增加。至於調控cytochrome c釋放的Bax、Bcl-2及p53等蛋白質的表現,在三種細胞中均有不同的表現量變化,在LNCaP細胞中,此三種蛋白的表現量沒有顯著性的差別,但在DU145及PC3細胞中,此三種蛋白質可在硫蜂斗菜素及異硫蜂斗菜素的刺激之下,改變其蛋白含量,調控粒線體內膜中cytochrome c的釋出。除了上述蛋白質的變化,在硫蜂斗菜素及異硫蜂斗菜素的刺激之下,PARP亦有明顯的截切現象,顯示著細胞凋亡的發生。觀看硫蜂斗菜素及異硫蜂斗菜素對於三種人類前列腺癌細胞株之IC50,硫蜂斗菜素對於人類前列腺癌細胞株的抑制生長效果比異硫蜂斗菜素強,並且硫蜂斗菜素及異硫蜂斗菜素對於人類前列腺癌細胞株之細胞倍增時間的抑制效應,遠大於其對於小鼠TM3萊氏細胞株以及人類腎上腺皮質癌細胞株(h295)的影響,亦即表示,相較於其他種細胞株,硫蜂斗菜素及異硫蜂斗菜素可有效的對人類前列腺癌細胞造成細胞凋亡、抑制細胞增殖,且具有相當的特異性。硫蜂斗菜素及異硫蜂斗菜素對於治療前列腺癌的潛力是未來相當值得研究的議題。
S-petasin and iso-S-petasin are bioactive compounds isolated from leaves or roots of Petasites hybridus (Engl. Butterbur; German Pestwure) which has been used therapeutically for more than 2000 years in Greek. It has been reported that the leaf and root extracts of Petasites hybridus relieve gastrointestinal pain, lung-disease such as asthma and cough, as well as spasms of the urogenital-tract, and even suppress the proliferation of human T24 bladder carcinoma cells. In 2000, S-petasin had been found to decrease the testosteron releasing by rat testicular interstitial cells. But few studies about S-petasin and iso-S-petasin on prostate cancer cells have been performed. Prostate cancer has become the most frequently diagnosed, noncutaneous neoplasm and the second leading cancer-related death in the United States. However, during the past 10 years, prostate cancer becomes a more common cancer in Asia. In this study, three prostate cancer cell lines, LNCaP, DU145 and PC3 were used to evaluate the anti-proliferation effects and the underlying mechanisms of S-petasin and iso-S-petasin. MTT assay, trypan blue exclusion, doubling time testing, light microscopic photograph, western blot and a colorimetric assay for caspases were employed in the present study. When MTT assay combined with trypan blue exclusion and doubling time testing, the decrease of cell number caused by S-petasin and iso-S-petasin was conspicuous. Light microscopic photographs of DU145 and PC3 showed that cell became rounded up, shrank and detached from the bottom of the plate. The LNCaP cells didn’t shrink, but showed a rounded up morphology. Protein expressions of apoptosis modulators, such as caspases, PARP, p53, Bcl-2, mitochondrial Bax, cytosolic cytochrome c were analyzed by western blot and colorimetric assays. Results indicated that cytochrome c released from mitochondria in three cell lines. However only p53, mitochondrial Bax and Bcl-2 showed significant changes in DU145 and PC3 cells,. Increase of active form of caspases and decrease of procaspases were also significant in three cell lines. Indeed, PARP was cleaved in the three prostate cancer cell lines when challenged with S-petasin and iso-S-petasin. Moreover, the IC50 of S-petasin on prostate cancer cell lines was lower than that of iso-S-petasin. In addition, the S-petasin or iso-S-petasin induced cell growth inhibition in three prostate cancer cell lines were much higher than that found in mouse TM3 Leydig cells and in human adrenal cortical carcinoma cells ( h295 ). These results suggest that S-petasin and iso-S-petasin selectively suppress the proliferation of androgen-dependent and androgen-independent prostate cancer cell lines by causing apoptosis. The potential of using S-petasin or Iso-S-petasin for treatment of prostate cancer is worthy of further investigation.
1. Aebi, A., J. Buchi, T. Waaler, E. Eichenberger, and J. Schmutz. Constituents of Petasites hybridus (L) FI. Wett. I. Pharm. Acta. Helv. 30:277-279, 1955.
2. Altman F. P. Tetrazolium salts and formazans. Prog. Histochem. Cytochem. 9: 1-56, 1976.
3. Berger, D, W. Burkard, and W. Schaffner. Influence of Petasites hybridus on dopamine-D 2 and histamine-H 1 receptors. Pharm. Acta. Helv. 72:373–375, 1998.
4. Bickel, D, T. Roder, H. J. Bestmann, and K. Brune. Identification and characterization of inhibitors of peptido-leukotriene-synthesis from Petasites hybridus. Planta. Med. 60: 318-322, 1994.
5. Boldin M. P., T. M. Goncharov, Y. V. Goltsev, D. Wallach. Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death. Cell. 85: 803-815, 1996.
6. Boone, C. W., G. J. Kelloff, and W. E. Malone. Identification of candidate cancer chemopreventive agents and their evaluation in animal models and human clinical trials: a review. Cancer Res. 50: 2-9, 1990.
7. Bruchovsky, N., B. Lesser, E. Van Doorn, and S. Craven. Hormonal effects on cell proliferation in rat prostate. Vitam. Horm. 33: 61-102, 1975.
8. Brune, K., D. Bickel, and B. A. Peskar. Gastro-protective effects by extracts of Petasites hybridus: the role of inhibition of peptido-leukotriene synthesis. Planta. Med. 59: 494-496, 1993.
9. Bucher, K. An antispastic principle in Petasites officinalis Moench. Naunyn Schmiedebergs Arch. Exp. Pathol. Pharmakol. 213: 69-71, 1951.
10. Budihardjo, I., H. Oliver, M. Lutter, X. Luo, and X. Wang. Biochemical pathways of caspase activation during apoptosis. Annu. Rev. Cell Dev. Biol. 15: 269-290, 1999.
11. Bunz, F., A. Dtriaux, C. Lengauer, T. Waldman, S. Zhou, J. P. Brown, J. M. Sedivy, K. W. Kinzler, and B. Vogelstein. Requirement for p53 and p21 to sustain G2 arrest after DNA damage. Science 282: 1497-1501, 1998.
12. Burdon R. H., Gill V., and Rice-Evens C. Reduction of a tetrazolium salt and superoxide generation in human tumor cells ( Hela ). Free Radic. Res. Commun. 18: 369-380, 1993.
13. Cancer facts and figures 2002. New York: American Cancer Society, Inc., 3-15, 2002.
14. Chan, L., and B. W. O''Malley. Mechanism of action of the sex steroid hormones. N. Engl. J. Med. 294: 1322-1328, 1976.
15. Chang, C. K., H. J. Yu, K. W. Chan, and M. K. Lai. Secular trend and age-period-cohort analysis of prostate cancer mortality in Taiwan. J. Urol. 158: 1845-1848, 1997.
16. Chen, Y., and M. Z. Lai. c-Jun NH2-terminal kinase activation leads to a FADD-dependent but Fas ligand-independent cell death in Jurkat T cells. J. Biol. Chem. 276: 8350-8357, 2001.
17. Chu, T. M. Prostate-specific antigen and early detection of prostate cancer. Tumour Biol. 18: 123-134, 1997.
18. Debmimer, B. and B. Meier. Study on clinical properties and mechanism of action of Petasites in bronchial asthma and chronic obstructive bronchitis. Pharmaceutica Acta. HelLetiae. 72:359-380, 1998.
19. de Launoit, Y., R. Kiss, V. Jossa, M. Coibion, R. J. Paridaens, E. De Backer, A. J. Danguy, and J. L. Pasteels. Influences of dihydrotestosterone, testosterone, estradiol, progesterone, or prolactin on the cell kinetics of human hyperplastic prostatic tissue in organ culture. Prostate 13: 143-153, 1998.
20. Denis, L., F. Keuppens, C. Mahler, F. M. Debruyne, E. H. Weil, G. Lunglmayr, D. Newling, M. R. Robinson, B. Richards, P. H. Smith, and et al. Long term therapy with a depot LHRH analogue (Zoladex) in patients with advanced prostatic cancer. Prog. Clin. Biol. Res. 243A: 221-227, 1987.
21. di Sant''Agnese, P. A. and Neuroendocrine. Differentiation in human prostatic carcinoma. Hum. Pathol. 23: 287-296, 1992.
22. di Sant''Agnese, P. A., and K. L. de Mesy Jensen. Endocrine-paracrine (APUD) cells of the human female urethra and paraurethral ducts. J. Urol. 137: 1250-1254, 1987.
23. Edwards, A., H. A. Hammond, L. Jin, C. T. Caskey, and R. Chakraborty. Genetic variation at five trimeric and tetrameric tandem repeat loci in four human population groups. Genomics 12: 241-253, 1992.
24. Flora of Taiwan Editorial Committee, Flora of Taiwan. 1978.
25. Fraumeni, J. F., Jr., and T. J. Mason. Cancer mortality among Chinese Americans, 1950-1969. J. Natl. Cancer Inst. 52: 659-665, 1974.
26. Gann, P. H., C. H. Hennekens, and M. J. Stampfer. A prospective evaluation of plasma prostate-specific antigen for detection of prostatic cancer. JAMA 273: 289-294, 1995.
27. Glantz, G. M. Cirrhosis and carcinoma of the prostate gland. J. Urol. 91: 291-293, 1964.
28. Gleave, M. E., J. T. Hsieh, H. C. Wu, A. C. von Eschenbach, and L. W. Chung. Serum prostate specific antigen levels in mice bearing human prostate LNCaP tumors are determined by tumor volume and endocrine and growth factors. Cancer Res. 52: 1598-1605, 1992.
29. Goping, I. S., A. Gross, J. N. Lavoie, M. Nguyen, R. Jemmerson, K. Roth, S. J. Korsmeyer, and G. C. Shore. Regulated targeting of BAX to mitochondria. J. Cell. Biol. 143: 207-215, 1998.
30. Gordon, G. G., K. Altman, A. L. Southren, E. Rubin, and C. S. Lieber. Effect of alcohol (ethanol) administration on sex-hormone metabolism in normal men. N. Engl. J. Med. 295: 793-797, 1976.
31. Gottlieb, R. A., and D. J. Granville. Analyzing mitochondrial changes during apoptosis. Methods 26: 341-347, 2002.
32. Graham, S., B. Haughey, J. Marshall, R. Priore, T. Byers, T. Rzepka, C. Mettlin, and J. E. Pontes. Diet in the epidemiology of carcinoma of the prostate gland. J. Natl. Cancer Inst. 70: 687-692, 1983.
33. Green, D. R., and J. C. Reed. Mitochondria and apoptosis. Science 281: 1309-1312, 1998.
34. Greenlee, R. T., M. B. Hill-Harmon, T. Murray, and M. Thun. Cancer statistics. Ca: a Cancer J. Clin. 51: 15-36, 2001.
35. Gross, A., J. M. McDonnell, and S. J. Korsmeyer. Bcl-2 family members and the mitochondria in apoptosis. Gene Dev. 13: 1899-1911, 1999.
36. Haenszel, W., and M. Kurihara. Studies of Japanese migrants. I. Mortality from cancer and other diseases among Japanese in the United States. J. Natl. Cancer Inst. 40:43-68, 1968.
37. Hara, I., H. Miyake, S. Hara, S. Arakawa, and S. Kamidono. Differential involvement of the Fas receptor/ligand system in p53-dependent apoptosis in human prostate cancer cells. Prostate 45: 341-349, 2000.
38. He, M., P. S. Rennie, V. Dragowska, C. C. Nelson, and W. Jia. A mutant p53 can activate apoptosis through a mechanism distinct from those induced by wild type p53. FEBS Lett. 517: 151-154, 2002..
39. Hetts, S. W. To die or not to die: an overview of apoptosis and its role in disease. JAMA 279, 300-307, 1998.
40. Hill, P. B., and E. L. Wynder. Effect of a vegetarian diet and dexamethasone on plasma prolactin, testosterone and dehydroepiandrosterone in men and women. Cancer Lett. 7: 273-282, 1979.
41. Holinger, E. P., T. Chittenden, and R. J. Lutz. Bak BH3 peptides antagonize Bcl-xL function and induce apoptosis through cytochrome c-independent activation of caspases. J. Biol. Chem. 274: 13298-13304, 1999.
42. Hsing, A. W., L. Chang, A. M. Nomura, W. B. Isaacs, and H. K. Armenian. A glimpse into the future. Epidemiol. Rev. 23: 2, 2001.
43. Hsing, A. W., L. Tsao, and S. S. Devesa. International trends and patterns of prostate cancer incidence and mortality. Int. J. Cancer 85: 60-67, 2000.
44. Huang, T. G., S. M. Ip, W. S. Yeung, and H. Y. Ngan. Changes in p21WAF1, pRB, Mdm-2., Bax, and Bcl-2 expression in cervical cancer cell line transfected with a p53 expressing adenovirus. Eur. J. Cancer 36: 249-156, 2000.
45. Huggins, C., and C. V. Hodges. Studies on prostatic cancer. I. The effect of castration, of estrogen and androgen injection on serum phosphatases in metastatic carcinoma of the prostate. Ca: a Cancer J. Clin. 22: 232-240, 1972.
46. Jackson, M. A., B. S. Ahluwalia, J. Herson, M. Y. Heshmat, A. G. Jackson, G. W. Jones, S. K. Kapoor, J. Kennedy, J. Kovi, A. O. Lucas, E. O. Nkposong, E. Olisa, and A. O. Williams. Characterization of prostatic carcinoma among blacks: a continuation report. Cancer Treat. Rep. 61: 167-172, 1977.
47. Juniewicz, P. E., M. McCarthy, B. M. Lemp, T. A. Barbolt, C. Shaw, D. M. Hollenbaugh, R. C. Winneker, J. R. Reel, and F. H. Batzold. The effect of the steroidal androgen receptor antagonist, Win 49,596, on the prostate and testis of beagle dogs. Endocrinology 126: 2625-2634, 1990.
48. Karpinich, N. O., M. Tafani, R. J. Rothman, and M. A. Russo. The course of etoposide-induced apoptosis from damage to DNA and p53 activation to mitochondrial release of cytochrome c. J. Biol. Chem. 277: 16537-16552, 2002.
49. Keetch, D. W., J. P. Rice, B. K. Suarez, and W. J. Catalona. Familial aspects of prostate cancer: a case control study. J. Urol. 154: 2100-2102, 1995.
50. Kelloff, G. J., C. W. Boone, J. A. Crowell, S. G. Nayfield, E. Hawk, W. F. Malone, V. E. Steele, R. A. Lubet, and C. C. Sigman. Risk biomarkers and current strategies for cancer chemoprevention. J. Cell. Biochem. Suppl. 25: 1-14, 1996.
51. Koch H, and E. Steinegger. Spectrophotometric determination of condurangin. Pharm. Acta. Helv. 53:56-58, 1978.
52. Kuida, K., T. S. Zheng, S. Na, C. Kuan, D. Yang, H. Karasuyama, P. Rakic, and R. A. Flavell. Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice. Nature 384: 368-372, 1996.
53. Langer T, E. Mostl, R. Chizzola, and R. Gutleb. A competitive enzyme immunoassay for the pyrrolizidine alkaloids of the senecionine type. Planta. Med. 62:267-271, 1996.
54. Lee, C. Physiology of castration-induced regression in rat prostate. Prog. Clin. Biol. Res. 75A: 145-159, 1981.
55. Lee, C. T., and J. E. Oesterling. Diagnostic markers of prostate cancer: utility of prostate-specific antigen in diagnosis and staging. Semin. Surg. Oncol. 11: 23-35, 1995.
56. Levine, R.L., and M. Wilchinsky. Adenocarcinoma of the prostate: a comparison of the disease in blacks versus whites. J. Urol. 121: 761-762, 1979.
57. Lin H., C. H. Chien, Y. L. Lin, C. F. Chen, P. S. Wang. Inhibition of testosterone secretion by S-petasin in rat testicular interstitial cells. Chinese. J. Physiol. 43: 99-103, 2000.
58. Li, H., H. Zhu, C. J. Xu, and J. Yuan. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell 94: 491-501, 1998.
59. Luthi. I., U. Zweifel, P. Schmid, and C. Schlatter. Pyrrolizidin alkaloide in Petasites hybridus (L.) and Petasites albus L. Pharm. Acta. Helv. 88: 97-99, 1983.
60. Mancini, M., D. W. Nicholson, S. Roy, N. A. Thornberry, E. P. Peterson, L. A. Casciola-Rosen, and A. Rosen. The caspase-3 precursor has a cytosolic and mitochondrial distribution: implications for apoptotic signaling. J. Cell Biol. 140: 1485-1495, 1998.
61. Marumo, K., S. Baba, and M. Murai. Erectile function and nocturnal penile tumescence in patients with prostate cancer undergoing luteinizing hormone-releasing hormone agonist therapy. Int. J. Urol. 6: 19-23, 1999.
62. McNeal, J. E., E. A. Redwine, F. S. Freiha, and T. A. Stamey. Zonal distribution of prostatic adenocarcinoma. Correlation with histologic pattern and direction of spread. Am. J. Surg. Pathol. 12: 897-906, 1988.
63. Michel, P., R. Van Velthoven, M. Petein, S. Gras, C. Etievant, J. L. Pasteels, and R. Kiss. Influence of suramin alone or in combination with DHT and PDGF on the cell proliferation of benign and malignant human prostatic tissues in organ cultures. Anticancer Res. 11: 2075-2078, 1991.
64. Muzio M, A. M. Chinnaiyan, F. C. Kischkel, K. O''Rourke, A. Shevchenko, J. Ni, C. Scaffidi, J. D. Bretz, M. Zhang, R. Gentz, M. Mann, P. H. Krammer, M. E. Peter, V. M. Dixit. FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex. Cell 85: 817-827, 1996.
65. Noble, R. L. The development of prostatic adenocarcinoma in Nb rats following prolonged sex hormone administration. Cancer Res. 37: 1929-1933, 1977.
66. Oesterling, J. E. Prostate specific antigen: a critical assessment of the most useful tumor marker for adenocarcinoma of the prostate. J. Urol. 145: 907-923, 1991.
67. Oltvai, Z. N., C. L. Milliman, and S. J. Korsmeyer. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell 74: 609-619, 1993.
68. Ornstein, D. K., J. Oh, J. D. Herschman, and G. L. Andriole. Evaluation and management of the man who has failed primary curative therapy for prostate cancer. Urol. Clin. North. Am. 25: 591-601, 1998.
69. Panaro, N. J., N. C. Popescu, S. R. Harris, and U. P. Thorgeirsson. Flavone acetic acid induces a G2/M cell cycle arrest in mammary carcinoma cells. Br. J. Cancer 80: 1905-1911, 1999.
70. Partin, A. W., and J. E. Oesterling. The clinical usefulness of prostate specific antigen: update 1994. J. Urol. 152: 1358-1368, 1994.
71. Pienta, K. J., and P. S. Esper. Risk factors for prostate cancer. Ann. Intern. Med. 118: 793-803, 1993.
72. Reichardt, J. K., N. Makridakis, B. E. Henderson, M. C. Yu, M. C. Pike, and R. K. Ross. Genetic variability of the human SRD5A2 gene: implications for prostate cancer risk. Cancer Res. 55: 3973-3975,1995.
73. Ries, L. G., E. S. Pollack, and J. L. Young. Jr. Cancer patient survival: surveillance, epidemiology, and end results program, 1973-1979. J. Natl. Cancer Inst. 70: 693-707, 1983.
74. Rokhlin, O. W., G. A. Bishop, B. S. Hostager, T. J. Waldschmidt, S. P. Sidorenko, N. Pavloff, M. C. Kiefer, S. R. Umansky, R. A. Glover, and M. B. Cohen. Fas-mediated apoptosis in human prostate carcinoma cells. Cancer Res. 57: 1758-1768, 1997.
75. Ross, R., L. Bernstein, H. Judd, R. Hanisch, M. Pike, and B. Henderson. Serum testosterone levels in healthy young black and white men. J. Natl. Cancer Inst. 76: 45-48, 1986.
76. Scardino, P. T., R. Weaver, and M. A. Hudson. Early detection of prostate cancer. Hum. Pathol. 23: 211-222, 1992.
77. Scheidegger C., C. Dahinden, and U. Wiesmann. Effects of extracts and of individual components from Petasites on prostaglandin synthesis in cultured skin fibroblasts and on leucotriene synthesis in isolated human peripheral leucocytes. Pharm. Acta. Helv. 72:376-378, 1998.
78. Schuman, L. M., J. Mandel, C. Blackard, H. Bauer, J. Scarlett, and R. McHugh. Epidemiologic study of prostatic cancer: preliminary report. Cancer Treat. Rep. 61: 181-186, 1977.
79. Sellers, W. R., and D. E. Fisher. Apoptosis and cancer drug targeting. J. Clin. Invest. 104: 1655-1661, 1999.
80. Sherwood, E. R., C. J. Fong, C. Lee, and J. M. Kozlowski. Basic fibroblast growth factor: a potential mediator of stromal growth in the human prostate. Endocrinology 130: 2955-2963, 1992.
81. Shi, Y. Mechanisms of caspase activation and inhibition during apoptosis. Mol. Cell. 9: 459-470, 2002.
82. Siegenthaler, P. and M. Neuenschwander. Sesquiterpenes from P. hybridus (Furanpoetasin chemovar): Separation, isolation and quantitation of compounds from fresh plant extracts. Pharm. Acta. Helv. 72: 57-67, 1997.
83. Snowdon, D. A., R. L. Phillips, and W. Choi. Diet, obesity, and risk of fatal prostate cancer. Am. J. Epidemiol. 120: 244-250, 1984.
84. Snyder, B. W., R. C.Winneker, and F. H. Batzold. Endocrine profile of Win 49596 in the rat: a novel androgen receptor antagonist. J. Steroid Biochem. 33: 1127-1132, 1989.
85. Steinberg, G. D., B. S. Carter, T. H. Beaty, B. Childs, and P. C. Walsh. Family history and the risk of prostate cancer. Prostate 17: 337-347, 1990.
86. Thornberry, N. A., and Y. Lazebnik. Caspases: enemies within. Science 281: 1312-1316, 1998.
87. Vogelstein, B., D. Lane, and A. J. Levine. Surfing the p53 network. Nature 408: 307-310, 2000.
88. Wang, M. C., L. A. Valenzuela, G. P. Murphy, and T. M. Chu. Purification of a human prostate specific antigen. Invest. Urol. 17: 159-163, 1979.
89. Wilson, J. D. Recent studies on the mechanism of action of testosterone. N. Engl. J. Med. 287: 1284-1291, 1972.
90. Wolf B. B, and D. R. Green. Suicidal tendencies: apoptotic cell death by caspase family proteinases. J. Biol. Chem. 274: 20049-20052, 1999.
91. Yeh, J. Y., W. J. Huang, S. F. Kan, and P. S. Wang. Inhibitory effects of digitalis on the proliferation of androgen dependent and independent prostate cancer cells. J. Urol. 166: 1937-1942, 2001.
92. Yeh, J. Y., W. J. Huang, S. F. Kan, and P. S. Wang. Effects of bufalin and cinobufagin on the proliferation of androgen dependent and independent prostate cancer cells. Prostate 54: 112-124, 2003.
93. Zi, X., and R. Agarwal. Silibinin decreases prostate-specific antigen with cell growth inhibition via G1 arrest, leading to differentiation of prostate carcinoma cells: implications for prostate cancer intervention. Proc. Natl. Acad. Sci. U S A 96: 7490-7495, 1999.
94. Zi, X., A. W. Grasso, H. J. Kung, and R. Agarwal. A flavonoid antioxidant, silymarin, inhibits activation of erbB1 signaling and induces cyclin-dependent kinase inhibitors, G1 arrest, and anticarcinogenic effects in human prostate carcinoma DU145 cells. Cancer Res. 58: 1920-1929, 1998.
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