American ginseng and breast cancer therapeutic agents synergistically inhibit MCF-7 breast cancer cell growth

American ginseng and breast cancer therapeutic agents synergistically inhibit MCF-7 breast cancer cell growth
Duda RB, Zhong Y, Navas V, et al. American ginseng and breast cancer therapeutic agents synergistically inhibit MCF-7 breast cancer cell growth. Journal of Surgical Oncology. Volume 72, Issue 4, Pp. 230–9, December 1999
American ginseng (Panax quinquefolius L.) purportedly alleviates menopause symptoms because of putative estrogenicity.
Using a standardized American ginseng (AG) extract in MCF-7 breast cancer cells, the objectives were to evaluate the ability of AG to induce the estrogen- regulated gene pS2 by Northern blot analysis, determine the effect on cell growth using the MTT assay, and evaluate the cell cycle effects by flow cytometry.
AG and estradiol equivalently induced RNA expression of pS2. AG, in contrast to estradiol, caused a dose-dependent decrease in cell proliferation (P < 0.005). AG had no adverse effect on the cell cycle while estradiol significantly increased the proliferative phase (percent S-phase) and decreased the resting phase (G0–G1 phase) (P < 0.005). Concurrent use of AG and breast cancer therapeutic agents resulted in a significant (P < 0.005) suppression of cell growth for most drugs evaluated.
In vitro use of AG and breast cancer therapeutics synergistically inhibited cancer cell growth.

Chemopreventive Effects of Heat-processed Panax quinquefolius Root on Human Breast Cancer Cells

Wang C-Z, Aung HH, Zhang B, Sun S, Li X-L, He H, Xie J-T, He T-C, Du W & Yun C-S. Anticancer Res. 2008; 28(5A): 2545–51.
Former studies have shown that extract from American ginseng (Panax quinquefolius) may possess certain antiproliferative effects on cancer cells. In this study, the chemical constituents of both untreated and heat-processed American ginseng and their antiproliferative activities on human breast cancer cells were evaluated.
Materials and Methods
American ginseng roots were steamed at 120°C for 1 h or 2 h. The major ginsenosides in the two steamed and in the unsteamed extracts were quantitatively determined using high performance liquid chromatography (HPLC). The antiproliferative activities of these extracts and individual ginsenosides on MCF-7 and MDA-MB-231 breast cancer cells were assayed using the MTS method. The effects of the extracts and the ginsenosides on the induction of cell apoptosis, the expression of cyclins A and D1, and cell cycle arrest were evaluated.
Compared to the untreated extract, heat-processing reduced the content of ginsenosides Rb1, Re, Rc and Rd, and increased the content of Rg2 and Rg3. After 2 h steaming, the percent content of ginsenoside Rg3 was increased from 0.06% to 5.9%. Compared to the unsteamed extract, the 2 h steamed extract significantly increased the antiproliferative activity and significantly reduced the number of viable cells. The steamed extract also significantly reduced the expression of cyclin A and cyclin D1. The cell cycle assay showed that the steamed extract and ginsenoside Rg3 arrested cancer cells in G1-phase.
Heat-processing of American ginseng root significantly increases antiproliferative activity and influences the cell cycle profile.

Antiestrogenic effect of 20S-protopanaxadiol and its synergy with tamoxifen on breast cancer cells

Yu Y, Zhou Q, Hang Y, et al. Antiestrogenic effect of 20S-protopanaxadiol and its synergy with tamoxifen on breast cancer cells. Cancer. Volume 109, Issue 11, Pp. 2374–82, 1 June 2007
20S-protopanaxadiol (aPPD) is a major gastrointestinal metabolic product of ginsenosides. The latter share structural similarity with steroids and are the main pharmacologically active component in ginseng.
The authors investigated the interaction between aPPD and estrogen receptors (ER) in human breast adenocarcinoma MCF-7 cells through receptor binding assay, ER-induced gene expression, and cell proliferation both in vitro and in vivo.
aPPD, but not its close analog ginsenosides, competed with the [3H]-17-β estradiol (E2) for ER with IC50 at 26.3 μM. aPPD alone weakly induced luciferase reporter-gene expression controlled by an estrogen-regulated element, which was completely blocked by tamoxifen. aPPD alone, or in synergy with tamoxifen, blocked E2-induced transcriptional activation. aPPD also inhibited colony formation of endometrial cancer cells. aPPD potently inhibited estrogen-stimulated MCF-7 cell proliferation and synergistically enhanced the cytotoxicity of tamoxifen on both ER+ MCF-7 and ER− MDA-MB231 cells. Furthermore, aPPD, but not tamoxifen, inhibited Akt phosphorylation. Growth of MCF-7 xenograft tumor supplemented with E2 was completely inhibited in animals treated with aPPD, tamoxifen, or aPPD plus tamoxifen.
These results suggested that aPPD inhibits estrogen-stimulated gene expression and cell proliferation in ER-positive breast cancer cells. In addition, aPPD synergistically enhances cytotoxicity of tamoxifen in an ER-independent fashion, probably by down-regulating Akt activity. Our animal breast tumor model data showed that orally taken aPPD at 10mg/kg/day completely inhibited the growth of estrogen-supplemented breast cancer and was as effective as 3 mg/kg intraperitoneally administered tamoxifen.

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