20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Chung, Hyun Cheol

doi:10.3892/mmr.2010.328

Cited by 44 publications

(35 citation statements)

References 28 publications

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“…Zhou et al (23) showed that ginsenoside Rg3 can inhibit HepG2 cell proliferation by downregulating the expression of VEGF. Yuan et al (24) reported that the protein expression of anti-apoptotic Bcl2 was downregulated and the protein expression of pro-apoptotic P53 was upregulated by 20(S)-ginsenoside Rg3 in HT-29 colon cancer cells. The present study obtained similar results, which showed that P53 was upregulated, and BCL2 and VEGF were downregulated by treatment of the HepG2 cells with ginsenoside Rg3 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

Teng

Wang

et al. 2017

Molecular Medicine Reports

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Ginsenoside Rg3, a bioactive constituent isolated from Panax ginseng, exhibits antitumorigenic, antioxidative, antiangiogenic, neuroprotective and other biological activities are associated with the regulation of multiple genes. DNA methylation patterns, particularly those in the promoter region, affect gene expression, and DNA methylation is catalyzed by DNA methylases. However, whether ginsenoside Rg3 affects DNA methylation is unknown. High performance liquid chromatography assay, MspI/HpaII polymerase chain reaction (PCR) and reverse transcription-quantitative PCR were performed to assess DNA methylation. It was demonstrated that 20(S)-ginsenoside Rg3 treatment resulted in increased inhibition of cell growth, compared with treatment with 20(R)-ginsenoside Rg3 in the human HepG2 hepatocarcinoma cell line. It was additionally revealed that treatment with 20(S)-ginsenoside Rg3 reduced global genomic DNA methylation, altered cystosine methylation of the promoter regions of P53, B cell lymphoma 2 and vascular endothelial growth factor, and downregulated the expression of DNA methyltransferase (DNMT) 3a and DNMT3b more than treatment with 20(R)-ginsenoside Rg3 in HepG2 cells. These results revealed that the modulation of DNA methylation may be important in the pharmaceutical activities of ginsenoside Rg3.

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Section: Resultsmentioning

confidence: 99%

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

Teng

Wang

et al. 2017

Molecular Medicine Reports

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“…However, consistent with limited evidence for caspase activation, when the three cell types were treated with a general caspase inhibitor (zVAD-FMK), zVAD had only a slight effect on cell death induced by the combination of Rg 3 and doxorubicin (Figure 6A), indicating that the cells were primarily dying a caspase-independent cell death. Since we observed little caspase activation, and since Rg 3 has been previously reported to induce caspase activation in the colon cancer cell line HT-29 [52], we tested the Rg 3 and doxorubicin combination in this cell line to see if caspase activation would be more prevalent in this cell type. We were unable to detect either PARP or caspase-3 cleavage in these cells, and zVAD likewise failed to protect the cells from cell death (Figure S8B-C).…”

Section: Resultsmentioning

confidence: 99%

20(S)-Ginsenoside Rg3 is a novel inhibitor of autophagy and sensitizes hepatocellular carcinoma to doxorubicin

et al. 2014

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. High mortality from HCC is mainly due to widespread prevalence and the lack of effective treatment, since systemic chemotherapy is ineffective, while the targeted agent Sorafenib extends median survival only briefly. The steroidal saponin 20(S)-ginsenoside Rg3 from Panax ginseng C.A. Meyer is proposed to chemosensitize to various therapeutic drugs through an unknown mechanism. Since autophagy often serves as cell survival mechanism in cancer cells exposed to chemotherapeutic agents, we examined the ability of Rg3 to inhibit autophagy and chemosensitize HCC cell lines to doxorubicin in vitro. We show that Rg3 inhibits late stage autophagy, possibly through changes in gene expression. Doxorubicin-induced autophagy plays a protective role in HCC cells, and therefore Rg3 treatment synergizes with doxorubicin to kill HCC cell lines, but the combination is relatively nontoxic in normal liver cells. In addition, Rg3 was well-tolerated in mice and synergized with doxorubicin to inhibit tumor growth in HCC xenografts in vivo. Since novel in vivo inhibitors of autophagy are desirable for clinical use, we propose that Rg3 is such a compound, and that combination therapy with classical chemotherapeutic drugs may represent an effective therapeutic strategy for HCC treatment.

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“… 1 , 2 Rg3, one of ginsenosides derived from heat-processed ginseng, was found to be a potent inhibitor of tumor cell growth. 3 , 4 Rg3 induces apoptosis through generation of reactive oxygen species (ROS) in some cancer cells. 5 , 6 In our previous study, Rg3 induced the proteolytic cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP) in human breast cancer MDA-MD231 cells.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg3 Inhibits Constitutive Activation of NF-κB Signaling in Human Breast Cancer (MDA-MB-231) Cells: ERK and Akt as Potential Upstream Targets

Kim¹,

Kim²,

Park³

et al. 2014

J Cancer Prev

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Ginsenoside Rg3, one of the major ingredients of heat-processed ginseng, has been reported to inhibit the growth of various cancer cells. We previously reported that Rg3 inhibited the proliferation and induced apoptosis of breast cancer (MDA-MB-231) cells. In the present study, we have explored the mechanism underlying the anti-proliferative and proapoptotic effects of Rg3 in MDA-MB-231 cells, which have constitutively activated NF-κB and the mutant form of p53. Rg3 inhibited DNA binding and transcriptional activity of NF-κB and these effects were attributable to its suppression of IKKβ activity, degradation of IκBα and subsequent nuclear translocation of the p65 subunit of NF-κB. Similarly, the constitutive activation of ERK and Akt through phosphorylation was gradually reduced in MDA-MB-231 cells treated with Rg3. The pharmacological inhibitors of these kinases both U0126 (MEK1/2 inhibitor) and LY294002 (PI3K inhibitor) abrogated the NF-κB DNA binding activity in MDA-MB-231 cells. In addition, Rg3 treatment lowered the levels of the mutant p53 in concentration- and time-dependent manners. Rg3 also increased the association between p53 and its negative regulator Mdm2 in MDA-MB-231 cells. These findings suggest that Rg3 induced apoptosis in MDA-MB-231 cells, which is mediated by blocking NF-κB signaling via inactivation of ERK and Akt as well as destabilization of mutant p53.

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20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Cited by 44 publications

References 28 publications

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

20(S)-Ginsenoside Rg3 is a novel inhibitor of autophagy and sensitizes hepatocellular carcinoma to doxorubicin

Ginsenoside Rg3 Inhibits Constitutive Activation of NF-κB Signaling in Human Breast Cancer (MDA-MB-231) Cells: ERK and Akt as Potential Upstream Targets

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