Ginsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells

Thi, Trang; Moon, Jeong Yong; Song, Yeon Woo; Viet, Pham Quoc; Phuc, Pham Van; Lee, Jung Min; Yi, Tae–Hoo; Cho, Moonjae; Cho, Somi Kim

doi:10.1016/j.canlet.2012.01.045

Cited by 146 publications

(98 citation statements)

References 62 publications

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“…Other distinguishing factors may exist such as differences in the level of expression of metadherin, which aids in the adhesion of cancer cells to the endothelium, and confers an enhanced chemoresistance to the cells [48]. Recent evidence also suggests that autophagy is a prosurvival trait held by CSCs, which may also allow them to travel through much smaller vessels [49][50][51][52].…”

Section: Intravasation Transport and Extravasationmentioning

confidence: 99%

Involvement of Mesenchymal Stem Cells in Cancer Progression and Metastases

Chang¹,

Schwertschkow²,

Nolta³

et al. 2015

CCDT

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Mesenchymal stem/stromal cells (MSCs) are known to be the helpers for the healing of tissue damage, often referred to as ambulatory cells. However, MSCs are also recruited by cancer cells to similarly aid in tumor growth and progression. In this review, some of the key steps in cancer progression and metastases are described including the various steps in which MSCs participate and may play important roles. MSCs aid in cancer cells' ability to evade immune attack, while promoting tumor angiogenesis, even being counter-acting against chemotherapeutics and other drugs used to fight various cancers. Furthermore, MSCs participate in many of the crucial steps in invasion and metastasis, including stimulating the epithelial-mesenchymal transition (EMT) and induction of stem-like properties that allow cancer stem cells to increase their survivability through the circulation. These steps are described in detail. Differences between circulating tumor cells (CTCs) and cancer stem cells (CSCs) are discussed, along with descriptions of the formation of a pre-metastatic niche, the role of exosomes from both cancer cells and MSCs in metastasis and tumor reseeding (self-seeding). More and more, MSCs are being proposed as a promising tumor targeting drug-delivery tool. In order to fulfill this promise, further understanding of the precise roles that MSCs play in the process of cancer metastases must be achieved, in attempting to create remedies that will improve the outcome of available therapeutics.

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Section: Intravasation Transport and Extravasationmentioning

confidence: 99%

Involvement of Mesenchymal Stem Cells in Cancer Progression and Metastases

Chang¹,

Schwertschkow²,

Nolta³

et al. 2015

CCDT

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“…12,13) Ginsenoside Rb1, precursor of ginsenoside F2, has been reported to prevent apoptosis induced by external stimuli in human keratinocyte cells (HaCaTs) as well as to inhibit activation by DHT. 14,15) However, the effects of ginsenoside F2 on hair loss have not been reported.…”

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confidence: 99%

Ginsenoside F2 Reduces Hair Loss by Controlling Apoptosis through the Sterol Regulatory Element-Binding Protein Cleavage Activating Protein and Transforming Growth Factor-β Pathways in a Dihydrotestosterone-Induced Mouse Model

Shin

Park

Hwang

et al. 2014

Biological & Pharmaceutical Bulletin

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This study was conducted to test whether ginsenoside F2 can reduce hair loss by influencing sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) and the transforming growth factor beta (TGF-β) pathway of apoptosis in dihydrotestosterone (DHT)-treated hair cells and in a DHT-induced hair loss model in mice. Results for ginsenoside F2 were compared with finasteride. DHT inhibits proliferation of hair cells and induces androgenetic alopecia and was shown to activate an apoptosis signal pathway both in vitro and in vivo. The cell-based 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that the proliferation rates of DHT-treated human hair dermal papilla cells (HHDPCs) and HaCaTs increased by 48% in the ginsenoside F2-treated group and by 12% in the finasteride-treated group. Western blot analysis showed that ginsenoside F2 decreased expression of TGF-β2 related factors involved in hair loss. The present study suggested a hair loss related pathway by changing SCAP related apoptosis pathway, which has been known to control cholesterol metabolism. SCAP, sterol regulatory elementbinding protein (SREBP) and caspase-12 expression in the ginsenoside F2-treated group were decreased compared to the DHT and finasteride-treated group. C57BL/6 mice were also prepared by injection with DHT and then treated with ginsenoside F2 or finasteride. Hair growth rate, density, thickness measurements and tissue histotological analysis in these groups suggested that ginsenoside F2 suppressed hair cell apoptosis and premature entry to catagen more effectively than finasteride. Our results indicated that ginsenoside F2 decreased the expression of TGF-β2 and SCAP proteins, which have been suggested to be involved in apoptosis and entry into catagen. This study provides evidence those factors in the SCAP pathway could be targets for hair loss prevention drugs.

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“…Ginsenoside F2 can induce the apoptosis and inhibit the proliferative activity of breast cancer cells through activating intrinsic apoptosis pathway and mitochondrial dysfunction. Meanwhile, ginsenoside F2 can also induce the formation of acid vesicles and GFP-LC3-labeled autophagosomes and up-regulation of Atg7 expression, which indicates that ginsenoside F2 initiates autophagy of breast cancer cells (Mai et al, 2012). On the other hand, the application of ginsenoside F2 in the presence of autophagy inhibitor can strengthen F2-induced cell death.…”

Section: Ginsenosidesmentioning

confidence: 96%

Autophagy-associated Targeting Pathways of Natural Products during Cancer Treatment

Zhang¹,

Wang²,

Yang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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It is well known that conventional chemotherapy and radiation therapy can result in toxicity to both normal cells and tumor cells, which causes limitations in the application of these therapeutic strategies for cancer control. Novel and effective therapeutic strategies for cancers with no or low toxicity for normal cells are a high priority. Therefore, natural products with anticancer activity have gained more and more attention due to their favorable safety and efficacy profiles. Pre-clinical and clinical studies have demonstrated that several representative natural compounds such as resveratrol, epigallocatechin-3-gallate, curcumin, allicin and ginsenosides have obvious anticancer potential. In this article, we summarize autophagy-associated targeting pathways of such natural products for inducing the death of cancer cells, and discuss the core autophagic pathways involved in cancer treatments. Recent advances in the discovery, evaluation and exploitation of natural compounds as therapeutic agents for cancers will provide references and support in pre-clinical and clinical application of novel natural drugs for the treatment of primary and metastatic tumors in the future.

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Ginsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells

Cited by 146 publications

References 62 publications

Involvement of Mesenchymal Stem Cells in Cancer Progression and Metastases

Involvement of Mesenchymal Stem Cells in Cancer Progression and Metastases

Ginsenoside F2 Reduces Hair Loss by Controlling Apoptosis through the Sterol Regulatory Element-Binding Protein Cleavage Activating Protein and Transforming Growth Factor-β Pathways in a Dihydrotestosterone-Induced Mouse Model

Autophagy-associated Targeting Pathways of Natural Products during Cancer Treatment

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