Ginsenoside Rg3 attenuates tumor angiogenesis via inhibiting bioactivities of endothelial progenitor cells

Kim, Jae-Won; Jung, Sun Young; Kwon, Yi-Hong; Lee, Junhee; Lee, You Mie; Lee, Boo-Yong; Kwon, Sang‐Mo

doi:10.4161/cbt.19599

Cited by 74 publications

(48 citation statements)

References 39 publications

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“…33 Recently, He et al reviewed that Rg3 is a natural inhibitor of colon cancer stem cell proliferation by inducing apoptosis through caspase-9 and caspase-3 pathways. 34 Weber et al also stated that Rg3 is thought to inhibit the proliferation of cancer stem cells in brain glioma.…”

Section: F-rge Decreased Cancer Stem-like Cell Viabilitymentioning

confidence: 99%

Fermented Red Ginseng Extract Inhibits Cancer Cell Proliferation and Viability

Jeon

Lee

et al. 2015

Journal of Medicinal Food

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Red ginseng (Panax ginseng C.A. Meyer) is the most widely recognized medicinal herb due to its remedial effects in various disorders, such as cancers, diabetes, and heart problems. In this study, we investigated the anticancer effect of fermented red ginseng extract (f-RGE; provided by Jeonju Biomaterials Institute, Jeonju, South Korea) in a parallel comparison with the effect of nonfermented red ginseng extract (nf-RGE; control) on several cancer cell lines--MCF-7 breast cancer cells, HepG2 hepatocellular carcinoma cells, and reprogrammed MCF-7 cells (mimicking cancer stem cells). Cells were cultured at various concentrations of RGE (from 0.5 up to 5 mg/mL) and their viabilities and proliferative properties were examined. Our data demonstrate the following: (1) nf-RGE inhibited cell viability at ≥1 mg/mL for MCF-7 cells and ≥2 mg/mL for HepG2 cells, (2) in the presence of a carcinogenic agent, 12-O-tetradecanoylphorbol-13-acetate (TPA), nf-RGE treatment in combination with paclitaxel synergistically decreased MCF-7 as well as HepG2 cell viability, (3) f-RGE (which contained a greater level of Rg3 content) more effectively decreased the viability of MCF-7 and HepG2 cells compared to nf-RGE, and (4) f-RGE appeared more potent for inhibiting cancerous differentiation of reprogrammed MCF-7 cells in a synergistic fashion with paclitaxel, especially in the presence of TPA, compared to nf-RGE. These findings suggest that f-RGE treatment may be more effective for decreasing cancer cell survival by inducing apoptotic cell death and also presumably for preventing cancer stem cell differentiation compared to nf-RGE.

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Section: F-rge Decreased Cancer Stem-like Cell Viabilitymentioning

confidence: 99%

Fermented Red Ginseng Extract Inhibits Cancer Cell Proliferation and Viability

Jeon

Lee

et al. 2015

Journal of Medicinal Food

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“…23,24) However the anticancer mechanisms of GRh2 and GRg3 to ALL cell lines remain unknown. In the present study, we observed that 20(S)-GRh2 is significantly more potent at inhibiting proliferation of human acute leukaemia line-Reh cells than GRg3, and that 20(S)-GRh2-induced apoptosis is mediated partially by caspase-dependent mitochondrial signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

20(<i>S</i>)-Ginsenoside Rh2 Induces Apoptosis in Human Leukaemia Reh Cells through Mitochondrial Signaling Pathways

Xia

Wang

et al. 2014

Biological & Pharmaceutical Bulletin

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“…As an antiangiogenic agent, ginsenoside Rg3 reduces VEGF expressions in cancer cells and attenuates the phosphorylation cascade of the VEGF-dependent p38/ERK signaling in vitro , which has also been confirmed in leukemia [12, 34, 35]. Moreover, obviously decreased VEGF expressions in tumor tissues are also found after treatment with ginsenoside Rg3 combined with gemcitabine [23].…”

Section: Discussionmentioning

confidence: 97%

Clinical benefit from EGFR-TKI plus ginsenoside Rg3 in patients with advanced non-small cell lung cancer harboring EGFR active mutation

Wang

Niu

et al. 2016

Oncotarget

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PurposeAcquired resistance is a bottleneck that restricts the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) for lung cancer. Ginsenoside Rg3 is an antiangiogenic agent which can down-regulate the expressions of vascular endothelial growth factor (VEGF) and EGFR. Combination of EGFR-TKI and ginsenoside Rg3 may be a promising strategy to delay acquired resistance. This retrospective study explored the efficacy and safety of this combined regimen in patients with EGFR mutation and advanced non-small cell lung cancer (NSCLC).ResultsBy the deadline of March 31th 2016, the median follow-up period reached 22.9 months. The median PFS was significantly longer in group A than in group B (12.4 months vs 9.9 months, P = 0.017). In addition, ORR was significantly higher in group A than in group B (59.6% vs 41.7%, P = 0.049). The median OS in group A showed no extended tendency compared with that in group B (25.4 months vs 21.4 months, P = 0.258). No significant difference in side effects was found between the two groups.MethodsA total of 124 patients with advanced NSCLC and EGFR active mutation were collected and analyzed. All of them were treated with first-line EGFR-TKI and divided into two groups. In group A (n=52), patients were administered EGFR-TKI plus ginsenoside Rg3 at standard doses. In group B (n=72), patients received EGFR-TKI alone. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR) and side effects were analyzed.ConclusionsGinsenoside Rg3 improves median PFS and ORR of first-line EGFR-TKI treatment in EGFR-mutant advanced NSCLC patients, thus providing a new regimen to delay acquired resistance of EGFR-TKI.

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Ginsenoside Rg3 attenuates tumor angiogenesis via inhibiting bioactivities of endothelial progenitor cells

Cited by 74 publications

References 39 publications

Fermented Red Ginseng Extract Inhibits Cancer Cell Proliferation and Viability

Fermented Red Ginseng Extract Inhibits Cancer Cell Proliferation and Viability

20(<i>S</i>)-Ginsenoside Rh2 Induces Apoptosis in Human Leukaemia Reh Cells through Mitochondrial Signaling Pathways

Clinical benefit from EGFR-TKI plus ginsenoside Rg3 in patients with advanced non-small cell lung cancer harboring EGFR active mutation

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