PC-SPES: A unique inhibitor of proliferation of prostate cancer cells in vitro and in vivo

Kubota, Tetsuya; Hisatake, Junichi; Hisatake, Yasuko; Said, Jonathan; Chen, Sophie S.; Holden, Stuart; Taguchi, Hirokuni; Koeffler, H. Phillip

doi:10.1002/(sici)1097-0045(20000215)42:3<163::aid-pros1>3.3.co;2-n

Cited by 3 publications

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“…Kubota et al [15] showed that the herbal mixture PC‐SPES (an herbal extract consisting of Isatis indigotica Fort, Panax pseudo‐ginseng Wall, Ganoderma lucidium Karst, Scutellaria baicauensis Georgi, Dendrantherma morifolium Tzvel, Glycyrrhiza galbra L., Rodosia rubescens , and Serenoa repens ) inhibits growth of human prostate cancer cells both in vivo and in vitro by causing cell cycle arrest. Some of the ingredients of this mixture have estrogenic activity.…”

Section: Introductionmentioning

confidence: 99%

2‐methoxyestradiol blocks cell‐cycle progression at G₂/M phase and inhibits growth of human prostate cancer cells

Kumar

Garcia

Slaga

2001

Molecular Carcinogenesis

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2-Methoxyestradiol (2-ME), an endogenous metabolite of 17beta-estradiol, is present in human blood and urine. Here we show for the first time that 2-ME significantly inhibited the growth of normal prostate epithelial cells and androgen-dependent LNCaP and androgen-independent DU145 prostate cancer cells. This growth inhibition was accompanied by a twofold increase in the G(2)/M population, with a concomitant decrease in the G(1) population, as shown by cell-cycle analysis. 2-ME treatment affected the cell-cycle progression of prostate cancer cells specifically by blocking cells in the G(2) phase. Immunoblot analysis of the key cell-cycle regulatory proteins in the G(2)/M phase showed a 14-fold increase in the expression of p21 and an eightfold increase in the expression of p34 cell division cycle 2 (cdc2). We also found an accumulation of phosphorylated cdc2 after 2-ME treatment. Furthermore, Wee 1 kinase was detectable after 2-ME treatment. 2-ME treatment also led to an increase in the activity of caspase-3, followed by apoptosis, as shown by terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate-biotin nick end-labeling and fluorescein isothiocyanate-poly(ADP-ribose) polymerase assay. Estrogen receptor levels did not change after treatment with 2-ME. Examination of the signaling pathways that mediate 2-ME-induced apoptosis showed reduction in the level of p53 expression and its DNA-binding activity. Given the fact that p53 mutations are common in patients with metastatic prostate cancer, our finding that 2-ME-mediated growth inhibition of human prostate cancer cells occurred in a p53-independent manner has considerable clinical significance. These findings, combined with the limited toxicity of 2-ME, may have significant implications for alternative treatment of advanced prostate cancer.

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Section: Introductionmentioning

confidence: 99%

2‐methoxyestradiol blocks cell‐cycle progression at G₂/M phase and inhibits growth of human prostate cancer cells

Kumar

Garcia

Slaga

2001

Molecular Carcinogenesis

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“…Patients reported a marked enhancement in their quality of life, with reduced pain, and falling PSA values. The side effects included enlargement of the breast and deep vein thrombosis [44][45][46][47][48][49][50][51][52]. However, the substance became contaminated with indomethacin and warfarin, and was withdrawn by manufacturers in the USA.…”

Section: Pc-spesmentioning

confidence: 99%

Complementary and alternative medicine in the treatment of prostate cancer

Auerbach

2006

The Journal of Men's Health & Gender

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Treatments based on complementary medicine have gained significant ground in oncology. Patients are mainly interested in adequate support, reduction of the side effects of clinical medicine, strengthening their immune system and enhancing quality of life both during and after chemotherapy and irradiation treatments. In the last few years, a number of complementary strategies for the treatment of prostate cancer have been evaluated and published in international journals. These studies allow us to present today, with scientific accuracy, the initial results of complementary treatment methods, describe their contraindications and interactions, and discuss a safe individualized therapy with the patient. In Western Europe and the USA, immunomodulatory, anti-oxidative and herbal therapies, in particular, have been investigated and published. Of these, we discuss mistletoe therapy, enzyme therapy, carotinoids, lycopene, vitamin A, C, E, selenium, phytoestrogens, PC-SPES, physical therapy and relaxation techniques and psychological therapy. Several studies have demonstrated the improvement in quality of life and the value of complementary medicine as an adjunct to chemotherapy or radiotherapy. Based on fruitful communication and cooperation with the treating oncological urologist, internist/oncologist or radiotherapist, complementary therapy might serve as a valuable and useful supportive measure for prostate cancer patients.

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The Prostate Journal Database

2000

Prostate J

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PC-SPES: A unique inhibitor of proliferation of prostate cancer cells in vitro and in vivo

Cited by 3 publications

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2‐methoxyestradiol blocks cell‐cycle progression at G₂/M phase and inhibits growth of human prostate cancer cells

2‐methoxyestradiol blocks cell‐cycle progression at G₂/M phase and inhibits growth of human prostate cancer cells

Complementary and alternative medicine in the treatment of prostate cancer

The Prostate Journal Database

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PC-SPES: A unique inhibitor of proliferation of prostate cancer cells in vitro and in vivo

Cited by 3 publications

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2‐methoxyestradiol blocks cell‐cycle progression at G2/M phase and inhibits growth of human prostate cancer cells

2‐methoxyestradiol blocks cell‐cycle progression at G2/M phase and inhibits growth of human prostate cancer cells

Complementary and alternative medicine in the treatment of prostate cancer

The Prostate Journal Database

Contact Info

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About

2‐methoxyestradiol blocks cell‐cycle progression at G₂/M phase and inhibits growth of human prostate cancer cells

2‐methoxyestradiol blocks cell‐cycle progression at G₂/M phase and inhibits growth of human prostate cancer cells