Anti-metastatic effects of ginsenoside Rd via inactivation of MAPK signaling and induction of focal adhesion formation

Yoon, Ji-Hae; Choi, Yoon-Hee; Cha, Seon‐Woo; Lee, Seong-Gene

doi:10.1016/j.phymed.2011.08.069

Cited by 55 publications

(42 citation statements)

References 24 publications

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“…Several other studies on anti-inflammatory and anti-cancer properties of American ginseng have focused on the ginsenoside or the saponin content of ginseng [64], [65], [66], [67], which is obtained from an aqueous ethanol extract (polar solvent) of ginseng. Of particular interest regarding our study, several studies have reported the anti-angiogenic and anti-metastatic properties of ginseng components [68], [69], [70], [71]. Ginsenoside 20(R) and 20(S)-Rg3 possess an ability to inhibit lung metastasis of tumor cells such as B16-BL6 melanoma and colon 26M3.1 by inhibition of adhesion and invasion of tumor cells and also by anti-angiogenesis activity [68].…”

Section: Discussionmentioning

confidence: 97%

“…Ginsenoside Rb2 inhibits invasion via MMP-2 suppression resulting in the inhibition of secondary spreading of uterine endometrial cancer [69]. Rd has been shown to inhibit migration of liver cancer cell lines HepG2 by reducing expression of MMP-1, MMP-2 and MMP-7 [70]. In contrast, ginsenoside Rg1 has been reported to promote and enhance angiogenesis and migration [72], [73], [74].…”

Section: Discussionmentioning

confidence: 99%

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A Key Role of microRNA-29b for the Suppression of Colon Cancer Cell Migration by American Ginseng

Poudyal

Cui

et al. 2013

PLoS ONE

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Metastasis of colon cancer cells increases the risk of colon cancer mortality. We have recently shown that American ginseng prevents colon cancer, and a Hexane extract of American Ginseng (HAG) has particularly potent anti-inflammatory and anti-cancer properties. Dysregulated microRNA (miR) expression has been observed in several disease conditions including colon cancer. Using global miR expression profiling, we observed increased miR-29b in colon cancer cells following exposure to HAG. Since miR-29b plays a role in regulating the migration of cancer cells, we hypothesized that HAG induces miR-29b expression to target matrix metalloproteinase-2 (MMP-2) thereby suppressing the migration of colon cancer cells. Results are consistent with this hypothesis. Our study supports the understanding that targeting MMP-2 by miR-29b is a mechanism by which HAG suppresses the migration of colon cancer cells.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

A Key Role of microRNA-29b for the Suppression of Colon Cancer Cell Migration by American Ginseng

Poudyal

Cui

et al. 2013

PLoS ONE

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“…Our results are supported by several lines of evidence indicating that ginseng inhibits MMP-2 and MMP-9 expression and activity; GE suppresses the metastasis of human hepatoma SK-Hep1 cells by inhibiting MMP-2 and MMP-9 [19], and GSs including Rb1, Rb2, Rd, and Rg3 inhibit MMP-2 and MMP-9 protein expression and activity in several types of cells such as SKOV-3 ovarian cancer cells and HepG2 human hepatoma cells [15–18, 30, 31], suggesting that the inhibition of MMP activity is important in terms of preventing cell metastasis. Although many reports indicated that ginseng prevents cell metastasis by inhibiting MMP activity, there is no evidence demonstrating that MMP inhibition by ginseng regulates adipogenesis.…”

Section: Discussionmentioning

confidence: 99%

Ginseng and Its Active Components Ginsenosides Inhibit Adipogenesis in 3T3-L1 Cells by Regulating MMP-2 and MMP-9

Lee

Park

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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The growth and development of adipose tissue are believed to require adipogenesis, angiogenesis, and extracellular matrix remodeling. As our previous study revealed that ginseng reduces adipose tissue mass in part by decreasing matrix metalloproteinase (MMP) activity in obese mice, we hypothesized that adipogenesis can be inhibited by ginseng and its active components ginsenosides (GSs). Treatment of 3T3-L1 adipocytes with Korean red ginseng extract (GE) inhibited lipid accumulation and the expression of adipocyte-specific genes (PPARγ, C/EBPα, aP2, and leptin). GE decreased both the mRNA levels and activity of MMP-2 and MMP-9 in 3T3-L1 cells. These effects were further inhibited by total GSs (TGSs) and individual GSs. TGSs and individual GSs also significantly decreased MMP-2 and MMP-9 reporter gene activities in the presence of phorbol 12-myristate 13-acetate (PMA), the MMP inducer. Among the GSs, Rb1 most effectively inhibited MMP activity. In addition, PMA treatment attenuated the inhibitory actions of GE and GSs on adipogenesis. Moreover, GE and GSs reduced the expression of NF-κB and AP-1, the transcription factors of MMP-2 and MMP-9. These results demonstrate that ginseng, in particular GSs, effectively inhibits adipogenesis and that this process may be mediated in part through the suppression of MMP-2 and MMP-9. Thus, ginseng and GSs likely have therapeutic potential for controlling adipogenesis.

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“…Recently, a study (Yoon et al, 2012) has shown that treatment with the Rd inhibits migration and invasion of the liver cancer cell line HepG2. This is accomplished by reducing the expression of MMP-1, MMP-2, and MMP-7, by blocking MAPK signaling, by inhibition of AP-1 activation, and by inducing focal adhesion formation and decreasing vinculin localization and expression.…”

Section: Molecular Mechanisms Of Anticancer Activities Of Ginseng Andmentioning

confidence: 99%

Ginsenosides as anticancer agents: In vitro and in vivo activities, structure–activity relationships, and molecular mechanisms of action

et al. 2012

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Conventional chemotherapeutic agents are often toxic not only to tumor cells but also to normal cells, limiting their therapeutic use in the clinic. Novel natural product anticancer compounds present an attractive alternative to synthetic compounds, based on their favorable safety and efficacy profiles. Several pre-clinical and clinical studies have demonstrated the anticancer potential of Panax ginseng, a widely used traditional Chinese medicine. The anti-tumor efficacy of ginseng is attributed mainly to the presence of saponins, known as ginsenosides. In this review, we focus on how ginsenosides exert their anticancer effects by modulation of diverse signaling pathways, including regulation of cell proliferation mediators (CDKs and cyclins), growth factors (c-myc, EGFR, and vascular endothelial growth factor), tumor suppressors (p53 and p21), oncogenes (MDM2), cell death mediators (Bcl-2, Bcl-xL, XIAP, caspases, and death receptors), inflammatory response molecules (NF-κB and COX-2), and protein kinases (JNK, Akt, and AMP-activated protein kinase). We also discuss the structure-activity relationship of various ginsenosides and their potentials in the treatment of various human cancers. In summary, recent advances in the discovery and evaluation of ginsenosides as cancer therapeutic agents support further pre-clinical and clinical development of these agents for the treatment of primary and metastatic tumors.

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Anti-metastatic effects of ginsenoside Rd via inactivation of MAPK signaling and induction of focal adhesion formation

Cited by 55 publications

References 24 publications

A Key Role of microRNA-29b for the Suppression of Colon Cancer Cell Migration by American Ginseng

A Key Role of microRNA-29b for the Suppression of Colon Cancer Cell Migration by American Ginseng

Ginseng and Its Active Components Ginsenosides Inhibit Adipogenesis in 3T3-L1 Cells by Regulating MMP-2 and MMP-9

Ginsenosides as anticancer agents: In vitro and in vivo activities, structure–activity relationships, and molecular mechanisms of action

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